PubMed Trending Research Digest — July 19, 2026

Automated digest · 99 articles · 15 research areas · July 19, 2026

Overview

This week’s papers cluster around two major frontiers: (1) immune regulation across tissues and diseases, and (2) precision biology—using multi-omics, spatial mapping, and engineered interventions—to identify actionable mechanisms.

On the immune side, multiple studies dissect how immune cells tune inflammation versus tolerance. Work on dendritic cell homeostasis links the unfolded protein response sensor IRE1 to steady-state maturation after apoptotic cell engulfment, suggesting a checkpoint for immune tolerance. In neurodegeneration, single-cell/spatial analyses show that microglial “reactivity” can vary substantially across disease models while vascular transcriptional programs remain more stable, and mechanistic studies connect AD risk biology (e.g., CD33M–clusterin interactions) to impaired microglial amyloid clearance. In cancer, several papers emphasize how immune suppression is built by the microenvironment—through fibroblast signaling circuits (e.g., CD248/periostin/ITGB1; IGF2-driven antigen presentation defects), ferroptosis-suppressive tumor states, and spatially organized immune niches (e.g., tertiary lymphoid structures in HCC).

On the precision biology side, the digest highlights mechanistic and translational strategies that move beyond correlations. Structural and biochemical GPCR studies map conformational landscapes underlying signaling bias and clarify how β-arrestin recruitment can physically couple to G proteins—guiding rational ligand design. In oncology, multi-omic and spatial approaches identify prognostic/response biomarkers (e.g., RPLP0 in ccRCC; TLS architecture in HCC; ferroptosis-suppressive signatures in bladder cancer), while functional profiling and longitudinal sampling aim to predict or overcome resistance to cell therapies (e.g., CAR-T durability limits driven by anti-CAR immunity in glioma; image-based immune phenotyping for myeloma bispecifics). Finally, several studies connect systemic physiology to disease risk—ranging from metabolic biomarker trajectories and frailty proteomics to ECM stiffness directing lung fate and stromal BMP signaling protecting gastric stem cell genome integrity—underscoring a broader theme that “context” (niche, mechanics, spatial organization, and time) is increasingly central to mechanism and prediction.

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Adult neurogenesis and brain development programs

Robust regulatory interplay of enhancers, facilitators, and promoters in a native chromatin context.

Using a recombinase-mediated genome-rewriting platform at a native human chromatin locus, this study dissected how the long-range enhancer eNMU regulates its target gene Neuromedin U (NMU) with endogenous enhancer architecture. The key finding was that eNMU contains two functionally distinct sub-elements—an autonomous enhancer (e1) and an intrinsically inactive facilitator (e2)—where e2 robustly augments e1 to achieve ~10,000-fold activation of NMU. This provides a mechanistic framework for how enhancer–facilitator–promoter interactions operate in native chromatin and can inform gene-regulatory therapeutic design.

Zhou Z, Cheng Y, Lieberth J et al. · Cell · (2026) · View on PubMed ↗

Skin-innervating glutamatergic neurons modulate aging.

This study investigated how skin-innervating glutamatergic neurons influence aging by comparing young versus aged skin and manipulating neuronal inputs in vivo, focusing on neurofilament heavy chain (Nefh) in Vglut2+ neurons. Cutaneous denervation and Nefh deletion in Vglut2+ glutamatergic neurons accelerated skin aging by inducing fibroblast senescence and collagen loss, while glutamate supplementation improved aging phenotypes. The results identify a neuron–fibroblast signaling axis that could be targeted to slow or reverse age-associated skin deterioration.

Wang Z, Jin X, Wu Y et al. · Cell · (2026) · View on PubMed ↗

Therapeutic Gene Editing of APOE4 in Sporadic Alzheimer’s Disease via Prime Editor 7.

This study developed an APOE4 allele–specific prime editing strategy in the context of sporadic Alzheimer’s disease, using optimized APOE4-targeting pegRNA and Prime Editor 7 (PE7) to convert APOE4 to APOE3. PE7 achieved robust, specific APOE4-to-APOE3 editing with no detectable off-target effects, reducing ApoE4 protein levels and attenuating key Alzheimer’s disease–related phenotypes. These results support prime editing as a precision therapeutic approach to directly correct the strongest genetic risk factor for sporadic AD by functionally replacing APOE4 with the lower-risk APOE3 variant.

Kim Y, Lee G, An S et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

PUM1 and PUM2 promote translation of chromatin regulators to ensure mammalian spermatogenesis.

This study investigated how translational control couples to chromatin remodeling during mammalian spermatogenesis by analyzing the RNA-binding proteins PUMILIO1 (PUM1) and PUMILIO2 (PUM2) in the mouse testis. Conditional deletion of Pum1 and Pum2 in germ cells caused spermatogenic failure, defective nuclear shaping, impaired histone-to-protamine exchange, and complete male sterility, with polysome profiling and ribosome sequencing showing selective reductions in translation efficiency of chromatin regulator mRNAs. These results establish PUM1/PUM2 as key translational regulators that ensure proper chromatin regulator production for successful spermatogenesis.

Zang M, Liu S, Xie Z et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Paraspeckles as a target for myocardial hypertrophy.

This study investigated whether paraspeckles—membraneless organelles formed via long non-coding RNA Neat1 through liquid-liquid phase separation (LLPS)—contribute to pathological myocardial hypertrophy and heart failure. Using RNA fluorescence in situ hybridization (FISH) and related experimental approaches (details truncated), it tested the role of the Neat1/paraspeckle LLPS pathway in hypertrophic remodeling triggered by stress stimuli such as pressure overload or sympathetic activation. The work is significant because it proposes an RNA-mediated LLPS mechanism as a potential therapeutic target for preventing or treating cardiac hypertrophy and subsequent heart failure.

Pan J, Zhong G, Du R et al. · European heart journal · (2026) · View on PubMed ↗

Extracellular Vesicles From Human Fallopian Tubes Enhance IVF Embryo Development and Contain Functional Proteins Including YWHAZ.

This experimental study examined whether extracellular vesicles (EVs) derived from human fallopian tubes (oEVs) can be internalized by human preimplantation embryos and improve developmental outcomes in vitro. oEVs were rapidly taken up by embryos and increased developmental quality, including higher high-quality Day 3 embryo formation and blastocyst development, while label-free proteomics identified 6505 oEV proteins enriched for metabolic, antioxidant, and stress-response pathways. The findings are clinically relevant for IVF because they support a functional, protein-carrying EV cargo that may enhance early embryogenesis and redox balance.

Li Y, Xiong W, Gao L et al. · Journal of extracellular vesicles · (2026) · View on PubMed ↗ · Free PDF ↗

In vivo multimodal PET/MRI imaging and plasma biomarkers implicate glymphatic dysfunction linking neuroinflammation to tau pathology in the early Alzheimer’s disease continuum.

This multimodal imaging and biomarker study in 355 ADNI participants plus 59 from Wuhan Union Hospital investigated links among neuroinflammation, glymphatic dysfunction, and tau pathology across the early Alzheimer’s disease continuum. Using 18F-AV1451 tau PET and glymphatic dysfunction estimation via diffusion tensor image analysis along the perivascular space (DTI-ALPS), the authors report that in vivo PET/MRI measures and plasma biomarkers implicate glymphatic dysfunction as a mechanistic bridge between neuroinflammation and tau pathology. The findings are significant because they suggest glymphatic impairment may be a targetable pathway connecting inflammatory processes to tau accumulation early in AD.

Xu X, Liu D, Sun X et al. · European journal of nuclear medicine and molecular imaging · (2026) · View on PubMed ↗

Functional immune profiling translates T cell dynamics into predictive biomarkers for myeloma immunotherapy.

This study developed an image-based, high-content ex vivo assay using patient-derived bone marrow mononuclear cells from relapsed/refractory multiple myeloma patients treated with the BCMA TCE teclistamab or the GPRC5D TCE talquetamab. It identified three functional response phenotypes—non-responder, cytotoxic, and cytotox—by multiplex immunofluorescence quantifying plasma cell lysis, T cell expansion/morphology, and spatial T cell–plasma cell engagement. These functional immune profiling biomarkers could enable earlier prediction of which myeloma patients will respond to BCMA- or GPRC5D-directed bispecific T cell engager therapy.

Herzberg F, Lu F, Korenkov M et al. · Leukemia · (2026) · View on PubMed ↗ · Free PDF ↗

Developmental priming of adult proteostasis and longevity by NuA4 complex activity in early life.

This study used the genetically tractable, long-lived model organism C. elegans to test whether early-life modulation of the TIP60/NuA4 acetyltransferase complex programs adult proteostasis and longevity. Reducing NuA4/TIP60 activity during a critical early-life window enduringly enhanced proteostasis and extended lifespan, mechanistically involving depletion of H4K16ac and an early-life-biased, XBP-1-mediated unfolded protein response. The work supports developmental “proteostasis priming” as a causal mechanism for long-term lifespan extension and suggests early-life targeting of proteostasis pathways could influence aging trajectories.

Wang Y, Xiong X, Zhang R et al. · The EMBO journal · (2026) · View on PubMed ↗ · Free PDF ↗

Integrated 5-HT2A-TrkB and G protein signaling in serotonergic psychedelic responses.

This study investigated how serotonergic psychedelic signaling integrates 5-HT2A and TrkB pathways using a neural stem cell-derived in vitro model differentiated into neuronal and glial lineages. It applied molecular pharmacology across a panel of tryptamines, phenethylamines, and ergolines (including psychedelic and non-psychedelic analogs) to dissect integrated 5-HT2A–TrkB and G protein signaling in psychedelic responses. The findings provide a mechanistic framework linking acute serotonergic psychedelic receptor signaling to downstream neuroplasticity-relevant pathways.

Taddei-Tardón M, Medina-Rodríguez L, Maltman JL et al. · Molecular psychiatry · (2026) · View on PubMed ↗

Pioneer transcription factors direct tissue-specific cohesin chromatin entry and three-dimensional genome organization.

This study examined how pioneer transcription factors regulate tissue-specific cohesin chromatin entry by focusing on the cohesin loader NIPBL and its recruitment mechanisms. Using motif analysis and chromatin immunoprecipitation-sequencing, it showed that NIPBL is prepositioned at tissue-specific sites largely distinct from CTCF/cohesin binding, with FOXA1 directing NIPBL to intratopologically associating domain regions for symmetric loop extrusion and ETS factors guiding NIPBL to TAD boundaries for asymmetric extrusion. These results clarify how pioneer factors establish tissue-specific 3D genome organization by controlling where cohesin loads and how loops are extruded.

Wang S, Zhang X, Jia T et al. · Nature genetics · (2026) · View on PubMed ↗

A neuroprosthesis for restoring hand movement and sensation in a person with complete tetraplegia.

This report describes a double neural bypass (DNB) neuroprosthesis in a person with complete tetraplegia, combining an intracortical brain-computer interface with targeted, patterned neuromodulation of the spinal cord and cortex. The system enabled real-time control of the user’s own hand movement and promoted longer-term sensorimotor recovery that persisted even after the device was turned off. Clinically, this provides proof-of-concept for a hybrid brain–spinal–cortical approach to restore both movement and sensation after severe spinal cord injury.

Chandrasekaran S, Wandelt SK, Jangam A et al. · Nature medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Brown fat-specific RNA labelling reveals a network of inter-organ communication by secreted microRNAs.

This study used brown fat-specific RNA labeling in male mice via uracil phosphoribosyltransferase-mediated incorporation of 4-thiouracil to map secreted microRNA (miRNA) transfer from brown adipose tissue (BAT) to other organs. BAT secreted miRNAs through small extracellular vesicles and plasma protein-associated compartments, and miRNAs from both routes showed tissue-selective uptake in liver, muscle, and hypothalamus; disrupting Dicer in BAT depleted miRNAs in BAT and distal tissues. These findings establish a mechanistic network of inter-organ communication by secreted miRNAs that can regulate systemic energy metabolism.

Lino M, Palermo-Ruiz G, Efthymiou V et al. · Nature metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

Single-nucleus analysis of the adult human olfactory epithelium uncovers shared neurogenesis programs with the brain.

Single-nucleus RNA-seq was used to profile the adult human olfactory epithelium from 6 living donors (145,720 nuclei) to define neurogenesis programs and compare them with brain neurogenesis. The study identified shared neurogenesis-related transcriptional programs between olfactory sensory neuron neurogenesis and brain neurogenesis, supported by integration with independent olfactory epithelium datasets. This provides a tractable in vivo human system to mechanistically study adult neurogenesis and its relevance to neurodevelopmental and neurodegenerative disease.

Song L, Fullard JF, Coleman C et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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GPCR structure, signaling bias, and arrestin–G protein coupling

β-arrestin recruitment facilitates a direct association with G proteins.

This study investigated the biochemical requirements for direct interactions between G proteins and β-arrestins in GPCR signaling using experimental approaches designed to test whether β-arrestin recruitment enables physical association with heterotrimeric G proteins. The key finding was that β-arrestin recruitment facilitates a direct association with G proteins, indicating that G protein and β-arrestin pathways can be coupled at the level of protein–protein interaction. This advances the mechanistic understanding of GPCR signaling integration, which may inform how GPCR-targeting drugs bias signaling outcomes.

Lee CY, Smith JS, Kohlmann T et al. · Nature communications · (2026) · View on PubMed ↗

Mechanistic insight into signal bias by the agonist-dependent conformational dynamics of GPR84.

Cryo-electron microscopy structures of the GPR84–Gi complex bound to the G protein–biased agonist DL-175 and of inactive GPR84 bound to the antagonist GLPG1205 were combined with signaling assays and molecular dynamics simulations. The authors mapped a conformational landscape that explains DL-175–dependent G protein bias and showed steric interactions that selectively block β-arrestin–associated conformational changes. These mechanistic insights support rational design of biased GPR84 ligands for immune/metabolic disorders.

Suzuki S, Tran DP, Nishikawa K et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Innate lymphoid cell (ILC) homeostasis and anti-tumor immunity

ASB2 inhibits lipid accumulation to promote ILC1 homeostatic fitness and anti-tumor immunity in the mouse liver.

The authors re-analyzed single-cell RNA-seq data from adult mouse liver and then used conditional ablation of Asb2 in NKp46+ cells to test how ASB2 controls ILC1 homeostasis and anti-tumor immunity in mice. ASB2 deficiency impaired ILC1 survival and reduced adult liver ILC1 numbers, with proteomics and bulk RNA-seq showing increased lipid metabolism and lipid storage in ASB2-deficient ILC1s. Targeting lipid synthesis to counteract ASB2-driven lipid accumulation may enhance ILC1-mediated anti-tumor immunity.

Bao B, Wang X, Chen Y et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Neuroinflammation, microglial reactivity, and vascular crosstalk in neurodegeneration

CD33 and clusterin interact biophysically and genetically to modulate Alzheimer risk.

This study combined structural and cellular experiments with genetic analyses to define how the Alzheimer’s disease (AD) risk-associated CD33M splice isoform interacts with clusterin (CLU) and modulates microglial function. CD33M ectodomain dimerization enabled binding of large multi-sialylated molecules, and CLU (± Aβ oligomers) bound CD33M with nanomolar avidity, triggering CD33M ITIM phosphorylation, SHP-1 recruitment, reduced Aβ phagocytosis, and impaired amyloid plaque clearance. These mechanistic data link CD33M:CLU interactions to impaired microglial amyloid clearance, providing a potential therapeutic target in AD.

Dodd RB, Enomoto M, Zhou Y et al. · Nature communications · (2026) · View on PubMed ↗

Involvement of TNFRSF9 in the Pathogenesis of Autoimmune Glial Fibrillary Acidic Protein Astrocytopathy.

This retrospective observational study examined CSF protein biomarkers of inflammatory activity, severity, and relapse risk in patients with autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy (GFAP-A), all of whom were CSF GFAP-IgG positive and had no alternative diagnosis. The key finding was the identification and validation of CSF protein biomarkers associated with GFAP-A disease activity and clinical outcomes (including relapse risk), although the abstract is truncated before listing specific proteins. Clinically, validated CSF biomarkers could improve monitoring and risk stratification in GFAP-A beyond GFAP-IgG alone, potentially guiding treatment intensity and relapse prevention.

Kimura A, Takekoshi A, Maekawa Y et al. · Neurology · (2026) · View on PubMed ↗

SORLA up-regulation suppresses pathological effects in aged tauopathy mouse brain.

This study tested whether up-regulating the trafficking receptor SORLA (Sortilin-related receptor containing LDLR class A repeats) can modify tau pathology in vivo using aged PS19 (P301S tau) transgenic mice. Transgenic SORLA up-regulation attenuated multiple tauopathy phenotypes, including tau phosphorylation and seeding, ventricle dilation, synapse loss, long-term potentiation impairment, and glial hyperactivation. The findings indicate that SORLA can suppress pathological effects in tau-driven neurodegeneration, supporting SORLA-based therapeutic strategies for aged tauopathy.

Huang H, Shi CH, Yang W et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Blood-based immunophenotyping of T cell profiles in patients with neurodegenerative disorders.

This study examined blood-based immunophenotyping of T-cell profiles across neurodegenerative disorders—Alzheimer’s disease, dementia with Lewy bodies, frontotemporal dementia, corticobasal syndrome, progressive supranuclear palsy—and aged-matched healthy controls. It found measurable differences in peripheral T-cell profiles among these conditions and explored associations between T-cell features and clinical measures of neurodegeneration/inflammation (as described in the abstract). The significance is that peripheral T-cell signatures may serve as accessible biomarkers and mechanistic clues for immune involvement in neurodegenerative dementias.

Malichova F, Swann P, Kigar SL et al. · Alzheimer’s research & therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Transplantation of human iPSC-derived microglia ameliorates neuropathology and circuit dysfunction in progranulin-deficient mice.

This preclinical study investigated whether transplanting human induced pluripotent stem cell (iPSC)-derived microglia into progranulin-deficient mice can rescue neurodegeneration, focusing on neuropathology and circuit dysfunction. It found that microglia replacement ameliorated disease-associated neuropathology and improved circuit function in the progranulin haploinsufficiency model, consistent with microglia being sensitive to progranulin loss and complement-driven pathology. The significance is that microglia-targeted cell therapy may be a viable strategy for familial FTD caused by progranulin deficiency.

Davtyan H, Naguib S, Voskobiynyk Y et al. · Molecular neurodegeneration · (2026) · View on PubMed ↗ · Free PDF ↗

Trained immunity links hematopoietic stem cell aging to aging-associated inflammation.

This mouse study investigated how hematopoietic stem cell (HSC) aging drives aging-associated inflammation via trained immunity, focusing on the mitochondrial deacetylase SIRT3. The key finding is that SIRT3 suppresses maladaptive trained immunity initiated by aging HSCs, and that SIRT3 overexpression in HSCs improves HSC function and attenuates age-related functional decline in distant tissues. Scientifically, it identifies SIRT3 as a mechanistic regulator linking HSC aging to chronic inflammation and trained-immunity-driven deterioration.

Mu WC, Barthez M, Feng Y et al. · Nature aging · (2026) · View on PubMed ↗ · Free PDF ↗

Microglia prune developing cortical blood vessels through PD-1 signaling.

This study examined microglia-mediated pruning of developing cortical blood vessels in postnatal day 11 mice using visualization and manipulation of microglia–vessel interactions. Microglia progressively approached cerebral vessels and mediated their pruning, with the PD-L1–PD-1 signaling axis identified as a key regulator. These results provide mechanistic insight into how immune cells shape cerebrovascular development and suggest PD-1 pathway involvement in vascular remodeling.

Zhang M, Wang Y, Yang R et al. · Nature neuroscience · (2026) · View on PubMed ↗

Brain-first and body-first subtypes of Lewy body disease.

This Nature Reviews Neurology article synthesizes evidence for the brain-first versus body-first (BvB) subtypes of Lewy body disease, proposing how Lewy pathology may originate in peripheral tissues versus the olfactory bulb. It argues that pathology can begin either in autonomic/gut or other peripheral neurons (body first) or in the olfactory bulb with spread to limbic regions (brain first), potentially triggered by exogenous factors such as infections or toxins. Scientifically, the BvB framework aims to unify heterogeneous clinical, imaging, and post-mortem pathology patterns and guide subtype-specific research and interventions.

Borghammer P, Van Den Berge N, Berg D et al. · Nature reviews. Neurology · (2026) · View on PubMed ↗

Heterogenous microglial reactivity contrasts with stable vascular transcriptional programs in mouse models of Alzheimer’s, CADASIL, and Traumatic Brain Injury.

Single-cell transcriptomics of mouse brain models of Alzheimer’s disease, CADASIL, and traumatic brain injury was used to compare microglial reactivity with stable vascular transcriptional programs across disease stages. The study found that microglial reactivity is heterogeneous across models while vascular programs remain comparatively stable, and it identified two previously unknown vascular endothelial subtypes. This clarifies how neuroinflammation-associated vascular changes differ from microglial state switching, informing interpretation of vascular contributions to neurodegenerative and vascular dementia-like disorders.

Bjørnholm KD, Li H, Del Gaudio F et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Dendritic cell homeostasis and immune tolerance checkpoints

The unfolded protein sensor IRE1 is essential for homeostatic dendritic cell maturation.

The unfolded protein response sensor IRE1 was tested for its role in homeostatic maturation of conventional type I dendritic cells (cDC1s) after apoptotic cell engulfment, focusing on LXRβ-dependent programs. Loss of IRE1 specifically impaired cDC1 (but not cDC2) homeostatic maturation and survival, and IRE1 activation depended on apoptotic cell uptake and cholesterol influx. The work links IRE1 to a steady-state, regulated IRE1-dependent decay program that supports cDC1 homeostasis, suggesting a new checkpoint for controlling immune tolerance versus inflammation.

Bosteels V, Maréchal S, Cloots E et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Innate antiviral immunity and interferon-pathway models

Empirical treatment with valganciclovir in infants living with HIV and hospitalised with severe pneumonia in Africa: a multicentre, open-label, factorial, randomised, controlled, superiority trial.

In a multicentre, open-label, 2×2 factorial randomized trial in infants aged 28–365 days hospitalized with severe HIV-associated pneumonia across six African countries, investigators tested whether empirical valganciclovir improves survival by targeting suspected cytomegalovirus. The key finding was that adding empirical valganciclovir to standard of care reduced mortality compared with standard of care alone (with factorial design also evaluating additional components). Clinically, this supports empiric CMV-directed therapy in high-risk settings to lower deaths in severe HIV-associated pneumonia.

Moraleda C, Tagarro A, Domínguez-Rodríguez S et al. · Lancet (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Purine and pyrimidine-based bacterial cyclic dinucleotides egress the phagosome and activate the innate immune sensor STING.

This mechanistic study in macrophages and murine tissues examined how bacterial cyclic dinucleotides (CDNs) trigger innate immune responses independently of Toll-like receptors, focusing on the STING pathway. The authors found that evolutionarily diverse bacterial CDNs activate STING after bacteriolysis in phagolysosomes in a process requiring two CDN transporters, driving TLR-independent type I interferon responses. Scientifically, it clarifies a common cytosolic sensing route for bacterial infection that could be leveraged to modulate interferon-driven inflammation.

Ragland SA, Lindblad KE, Li Y et al. · Immunity · (2026) · View on PubMed ↗

Macrophage-derived oxysterols organize T helper 2 cells to suppress type 1 inflammation during pulmonary fungal infection.

This study examined how macrophage-derived oxysterols spatially organize T helper 2 (TH2) cells to suppress type 1 inflammation during pulmonary fungal infection. It identified a cholesterol-derived chemotactic axis in which inflammation-expanded macrophages expressing CH25H produce 25-hydroxycholesterol, converted to 7α,25-dihydroxycholesterol that attracts GPR183-expressing TH2 cells into infectious lesions, thereby suppressing interferon-γ responsiveness in inflammatory Ly6C+ macrophages. Mechanistically, the work links macrophage oxysterol production to TH2 positioning and immune regulation, suggesting potential interventions to modulate harmful type 1 inflammation in fungal lung disease.

Zheng Y, Dobson HE, Jean Pierre M et al. · Science immunology · (2026) · View on PubMed ↗

The Parkinson’s disease-linked G2019S mutation of LRRK2 increases NADPH oxidase-2 activity in neutrophils for superior control of bacterial infections.

This study tested whether the Parkinson’s disease-linked LRRK2 p.G2019S mutation alters innate immune control of infection by evaluating neutrophils during mouse infections with Salmonella typhimurium or Listeria monocytogenes. The p.G2019S mutation increased NADPH oxidase-2 activity by promoting phosphorylation of p40phox and p47phox, driving their relocation to lysosomes and enhancing bacterial control. Immunologically, it links an LRRK2 Parkinson’s variant to improved neutrophil antimicrobial function, informing how LRRK2 signaling may influence infection susceptibility.

Hurley K, Kaul R, Yadav S et al. · Cellular & molecular immunology · (2026) · View on PubMed ↗

Juvenile hormone signaling acts during development and post-mating to suppress antibacterial defenses in Drosophila melanogaster.

This study in female Drosophila melanogaster examined how juvenile hormone (JH) signaling suppresses antibacterial defenses during development and after mating. It found that post-mating susceptibility depends on JH function across multiple life stages and target tissues, with mating inducing a rapid transient peak in JH titers followed by prolonged JH signaling. The results clarify the timing and tissue targets of JH-mediated immunosuppression, advancing understanding of how reproductive physiology trades off with immunity.

Keith SA, Gupta V, Kalukin AA et al. · Scientific reports · (2026) · View on PubMed ↗ · Free PDF ↗

Triple IFN pathway deficiency sensitizes mice to human respiratory virus infection independent of human viral receptor expression.

A triple interferon pathway–deficient mouse model (AGL) was generated by one-step knockout of IFNAR, IFNGR, and IFNLR, and its susceptibility to human respiratory viruses was assessed without relying on human viral receptor expression. AGL mice became susceptible to diverse human respiratory viruses, including adenovirus type 55 and monkeypox virus clade IIb, indicating that complete IFN pathway deficiency is sufficient to permit infection. This provides a broadly permissive preclinical model for studying human respiratory virus pathogenesis and for evaluating antiviral strategies targeting innate immunity.

Fan Q, Pan M, Jiang M et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Transposable elements, LINE-1 activity, and cancer genome instability

Multiomic profiling links L1 retrotransposition to genomic instability and ecDNA in bladder cancer.

Integrated multi-omic profiling was performed on a cohort of 48 bladder cancer patients using cell-free DNA sequencing, long-read tumor DNA sequencing, RNA-seq, and spatial transcriptomics to connect LINE-1 (L1) activity with genomic instability and extrachromosomal DNA (ecDNA). The study found frequent somatic LINE-1 insertions that are active and occur early in bladder cancer development, linking L1 insertion events to downstream genomic rearrangements and ecDNA formation. This supports a causal role for early L1 retrotransposition in driving genomic instability and clonal evolution in bladder cancer.

Pribus SJ, Osredek I, Otoničar J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Ferroptosis regulation and iron metabolism in cancer

Soulangianolide A targets FAM120A to disrupt SREBP1-driven lipid metabolic reprogramming and suppress clear cell renal cell carcinoma.

This study investigated the natural product Soulangianolide A (SA) in clear cell renal cell carcinoma (ccRCC) and tested whether it acts through FAM120A to disrupt SREBP1-driven lipid metabolic reprogramming. The key finding was that SA targeted FAM120A and suppressed SREBP1-dependent lipogenesis and associated malignant phenotypes, with functional validation using stable knockdown of SREBP1 or FAM120A in ccRCC models. This is significant because it identifies a FAM120A–SREBP1 lipid axis as a therapeutic vulnerability and supports SA as a candidate anti-ccRCC agent targeting tumor lipid metabolism.

Luo W, Song Z, Liu Z et al. · Journal of experimental & clinical cancer research : CR · (2026) · View on PubMed ↗ · Free PDF ↗

A ferroptosis-suppressive state drives resistance to bladder-preserving chemoradiotherapy in muscle-invasive bladder cancer.

This study profiled pretreatment tumors from 179 patients with muscle-invasive bladder cancer (MIBC) uniformly treated with bladder-preserving chemoradiotherapy (CRT) as part of trimodality therapy (TMT) and integrated bulk transcriptomics with immune features and outcomes. It identified a ferroptosis-suppressive transcriptional signature (FSS) associated with a resistance-associated tumor state and poorer response to CRT. The results suggest that ferroptosis suppression is a key mechanism of intrinsic resistance and could guide biomarker-driven or ferroptosis-targeted therapeutic strategies.

Tsujino T, Yamazaki S, Sakamoto M et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Lysosome as a central hub in ferroptosis-driven pathologies.

This review synthesizes evidence that lysosomes act as a central hub in ferroptosis-driven pathologies by coordinating iron metabolism and signaling events. It proposes a “lysosome–ferroptosis axis” linking metabolic signaling, autophagy, and lysosomal membrane permeabilization to ferroptosis execution across neurodegenerative, tumor, and cardiometabolic diseases. The framework highlights lysosomal processes as potential targets for therapeutic intervention in ferroptosis-related conditions.

Li S, Qiu B, Yi X et al. · Trends in molecular medicine · (2026) · View on PubMed ↗

Iron overload suppresses LKB1 and induces IL36G anti-tumor immunity in PDAC metastasis.

This study used CRISPR-based genetic screening in a pancreatic ductal adenocarcinoma (PDAC) liver metastasis model to identify metabolic vulnerabilities in the metastatic microenvironment, focusing on iron handling. Ferritin heavy chain (FTH1) emerged as a liver-specific dependency, and FTH1 loss suppressed tumor growth in the liver by disrupting iron handling and causing mitochondrial dysfunction and ionic imbalance. The work suggests that iron overload–linked pathways can be therapeutically targeted in PDAC metastasis, potentially exploiting FTH1/iron metabolism as a context-dependent anti-tumor liability.

Biancur DE, Venkatesh H, Crawford A et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

SUV39H2-mediated NCOA4 methylation controls ferritinophagy and ferroptosis in triple-negative breast cancer.

In triple-negative breast cancer, the authors investigated how the lysine methyltransferase SUV39H2 regulates the ferritinophagy cargo receptor NCOA4 to control ferritinophagy and ferroptosis. SUV39H2 mono-methylated NCOA4 at lysine 356, which reduced NCOA4 stability by enhancing NCOA4 interaction with the E3 ligase HERC2, promoting ubiquitination and proteasomal degradation. By modulating NCOA4 abundance and iron flux, this SUV39H2–NCOA4 axis identifies a potential targetable pathway to influence ferroptosis sensitivity in TNBC.

Liu L, Pei X, Li D et al. · Cell death & disease · (2026) · View on PubMed ↗ · Free PDF ↗

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Autophagy/lysosome pathways in neuropsychiatric disease

Withania somnifera (Ashwagandha) as an Adjunctive Treatment to Antipsychotic Medications for Patients With Schizophrenia.

This randomized, double-blind adjunctive trial studied Withania somnifera extract (WSE; Ashwagandha) added to antipsychotic medications in patients with schizophrenia who had a recent exacerbation, assessing symptoms with PANSS/CGI/PSS and measuring proinflammatory markers at baseline and 12 weeks. It found that WSE adjunct therapy improved schizophrenia outcomes versus placebo and was associated with reductions in proinflammatory markers (supporting an anti-inflammatory mechanism). The clinical significance is that Ashwagandha could be a low-cost adjunct to antipsychotics for symptom improvement in schizophrenia with an immunomodulatory pathway.

Marder SR, Kelly DL, DeVera G et al. · Journal of clinical psychopharmacology · (2026) · View on PubMed ↗ · Free PDF ↗

Perioperative outcomes in patients with myalgic encephalomyelitis/chronic fatigue syndrome undergoing general anesthesia: a retrospective matched-pair study.

This retrospective matched-pair study assessed perioperative outcomes in patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) undergoing general anesthesia compared with matched controls. The key finding is that ME/CFS patients experience measurable perioperative response differences (with the study designed to quantify outcomes and identify clinically relevant perioperative considerations). The results are significant for improving perioperative risk stratification and guiding future prospective anesthesia-focused research in ME/CFS.

Steinkirchner FM, Kaufmann CK, Kraus RF et al. · BMC anesthesiology · (2026) · View on PubMed ↗ · Free PDF ↗

Evans Syndrome Predicts Progression to Antiphospholipid Syndrome and/or Systemic Lupus Erythematosus in Children with Persistent Antiphospholipid Antibodies: A Prospective Cohort Study with Up to 29 Years of Follow-up.

In a prospective cohort of children (<18 years) with persistent antiphospholipid (aPL) antibodies and hematologic non-criteria manifestations—including Evans syndrome—followed up for as long as 29 years, the study evaluated predictors of progression to antiphospholipid syndrome (APS) and/or systemic lupus erythematosus (SLE). The key finding is that Evans syndrome predicts later development of APS and/or SLE in this pediatric persistent-aPL population. Clinically, identifying Evans syndrome as a long-term risk marker can improve surveillance and early intervention strategies for children with persistent aPL.

Baca V, Hernández-López D, González-Muñiz S et al. · Arthritis & rheumatology (Hoboken, N.J.) · (2026) · View on PubMed ↗

Association of traumatic experiences with depressive symptoms among LGBTQ+ population in China.

This study used baseline data from 8,384 participants in the TREASURE cohort in Chengdu, China to examine how trauma exposure (adverse childhood experiences, lifetime trauma, and LGBTQ+-related adversities) is associated with depressive symptoms among LGBTQ+ people. Depressive symptoms were present in 30.2% of participants and were strongly associated with trauma exposure (adjusted odds ratio 11.00, 95% CI 7.39–16.39), showing a dose-response pattern. These findings highlight the clinical importance of screening for cumulative trauma and LGBTQ+-specific adversities to reduce depression risk in non-Western LGBTQ+ populations.

Yang J, Wang Y, Liu L et al. · Nature human behaviour · (2026) · View on PubMed ↗

Schizophrenia and bipolar disorder risk gene AKAP11 sustains cognitive function by regulating TFEB-mediated autophagy.

The study examined how schizophrenia/bipolar disorder risk gene AKAP11 (Akap11) regulates cognition by controlling TFEB-mediated autophagy, using acute Akap11 depletion in the mouse hippocampus and complementary in vitro neuronal and non-neuronal models. Akap11 depletion caused cognitive deficits with synaptic dysfunction and autophagy dysregulation, and AKAP11 was shown to regulate autophagy initiation and lysosomal activity. These findings mechanistically connect AKAP11 haploinsufficiency to impaired TFEB-autophagy pathways, offering a route to target autophagy for cognitive symptoms in SCZ/BD.

Deng Z, Kan Y, Liu J et al. · Cell death and differentiation · (2026) · View on PubMed ↗

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Host–virus interactions via RNA splicing factors

Exploitation of host U2AF1 and U2AF2 splicing factors facilitates mosquito-borne orthoflavivirus infection across species.

This mechanistic study investigated how the host splicing factors U2AF1 and U2AF2 facilitate mosquito-borne orthoflavivirus infection across species, using proteomic profiling of endoplasmic reticulum fractions from cells infected with dengue virus or Zika virus (ZIKV) and functional domain-mapping. It found that U2AF1–U2AF2 are critical at the viral protein synthesis stage, that specific U2AF1 domains (including the RS domain and Zn1) and most U2AF2 domains (excluding the RS domain) are required, and that disrupting U2AF1–U2AF2 interaction potently suppresses ZIKV infection. Scientifically, this identifies a conserved host splicing-factor dependency that could be exploited for broad-spectrum antiviral strategies against orthoflaviviruses.

Huang C, Cai Y, Chen C et al. · Nucleic acids research · (2026) · View on PubMed ↗ · Free PDF ↗

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Clinical trials and real-world effectiveness of immunotherapies (oncology)

Prognostic impact of measurable residual disease in AML patients treated frontline with azacitidine and venetoclax: results from the French VENAURA registry.

This retrospective registry analysis studied 220 newly diagnosed acute myeloid leukemia (AML) patients treated frontline with azacitidine plus venetoclax (AZA/VEN) in the French VENAURA cohort, assessing measurable residual disease (MRD) by multiparametric flow cytometry (LAIP/LSC) and/or NPM1 RT-qPCR. Achieving MRD negativity at any time was strongly associated with improved overall survival, with cumulative MRD negativity observed in about 62–67% of patients. The results support MRD as a clinically actionable prognostic marker for AZA/VEN-treated AML outside clinical trials.

Heiblig M, Gross Z, Belhabri A et al. · Leukemia · (2026) · View on PubMed ↗ · Free PDF ↗

Real-world safety and effectiveness of enfortumab vedotin plus pembrolizumab in locally advanced or metastatic urothelial carcinoma: A multicenter Japanese cohort study.

This multicenter Japanese retrospective cohort study evaluated real-world safety and effectiveness of enfortumab vedotin plus pembrolizumab (EVP) as first-line treatment in locally advanced or metastatic urothelial carcinoma (la/mUC). The study assessed tumor response and survival outcomes (PFS, CSS, OS) alongside adverse events (AEs) using Kaplan–Meier methods and exploratory analyses for factors associated with outcomes. The findings provide practical evidence on how EVP performs and is tolerated in routine clinical care in Japanese patients.

Yanagisawa T, Iwatani K, Urabe F et al. · Urologic oncology · (2026) · View on PubMed ↗

Sub-Tenon’s triamcinolone bridging to adalimumab therapy in refractory noninfectious uveitic macular edema.

This retrospective longitudinal cohort study evaluated whether sub-Tenon’s triamcinolone acetonide (STTA) bridging improves outcomes when starting adalimumab (ADA) in 30 patients (44 eyes) with refractory noninfectious uveitic macular edema. Compared with ADA monotherapy, ADA plus STTA bridging was designed to provide earlier macular edema control during ADA’s delayed onset period. If confirmed by the reported outcomes, the strategy could offer a practical treatment optimization for refractory uveitic macular edema by reducing the time to disease control.

Zou Y, Yang M, Zhang J et al. · Graefe’s archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · (2026) · View on PubMed ↗ · Free PDF ↗

Asciminib monotherapy in patients with BCR::ABL1 T315I-mutated chronic-phase chronic myeloid leukemia: phase 1 trial final results.

This phase 1 trial reported long-term safety and efficacy of asciminib 200 mg twice daily in 48 patients with chronic-phase chronic myeloid leukemia harboring the BCR::ABL1 T315I mutation (NCT02081378). After a median 3.5 years of exposure, 53.3% of 45 evaluable patients achieved major molecular response (MMR), with continued on-treatment in many patients via posttrial access. The results support asciminib as an effective ABL1 myristoyl-pocket inhibitor option for T315I-mediated resistance in CML-CP.

Cortes JE, Rea D, Mauro MJ et al. · Leukemia · (2026) · View on PubMed ↗ · Free PDF ↗

Dose-reduced (24 Gy) involved-site radiotherapy combined with rituximab in early-stage non-gastric mucosa-associated lymphoid tissue lymphoma: a prospective phase II trial.

This prospective phase II study evaluated dose-reduced (24 Gy) involved-site radiotherapy combined with rituximab in 60 enrolled patients with early-stage non-gastric mucosa-associated lymphoid tissue (MALT) lymphoma. In the per-protocol efficacy-evaluable cohort (n=55), the combined immunoradiotherapy achieved a complete response rate of 100%, with only one distant recurrence observed at a median follow-up of 30.2 months. The regimen suggests that lowering ISRT dose while adding rituximab may maintain excellent local control and reduce distant relapse risk in early-stage non-gastric MALT lymphoma.

Liu H, Cheng Y, Liu S et al. · Leukemia · (2026) · View on PubMed ↗

Predictors of survival in adults with B-cell acute lymphoblastic leukemia treated with blinatumomab and/or inotuzumab ozogamicin in first salvage.

This retrospective analysis studied 172 adults with relapsed/refractory B-cell acute lymphoblastic leukemia treated in first salvage with blinatumomab and/or inotuzumab ozogamicin, assessing predictors of survival and the benefit of allogeneic HSCT after remission. Relapse within 12 months of initial diagnosis and measurable residual disease (MRD) positivity by multiparametric flow cytometry after cycle 1 were associated with worse relapse-free survival (RFS). The results help stratify which adults receiving B-cell-directed immunotherapies may benefit most from allo-HSCT based on early relapse timing and early MRD status.

Azevedo RS, Jabbour E, Jain N et al. · Leukemia · (2026) · View on PubMed ↗ · Free PDF ↗

Multidisciplinary approach to managing GPRC5D-related adverse events in relapsed or refractory multiple myeloma patients.

This article presents a multidisciplinary management framework for GPRC5D-related adverse events in relapsed/refractory multiple myeloma patients treated with talquetamab, a GPRC5D-targeting bispecific antibody. It synthesizes evidence to guide hematologists, oncology nurses, dieticians, and patients in preventing and managing characteristic oral toxicities (e.g., dysgeusia, dysphagia, dry mouth) and dermatologic/nail adverse events (e.g., rashes and skin-related symptoms). The recommendations aim to improve real-world tolerability and continuity of talquetamab therapy by standardizing supportive care for predictable GPRC5D-mediated toxicities.

Albrecht N, Boeckx E, Caers J et al. · Annals of hematology · (2026) · View on PubMed ↗ · Free PDF ↗

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Biomarkers, multi-omics, and spatial immune architecture in cancer

Multi-omics profiling highlights RPLP0 as a potential biomarker for prognosis and response to immunotherapy in clear cell renal cell carcinoma.

This study integrated bulk transcriptomics, proteomics, single-cell RNA-seq, and spatial transcriptomics to evaluate ribosomal protein lateral stalk subunit P0 (RPLP0) in clear cell renal cell carcinoma (ccRCC) using TCGA/GEO/ICGC/ArrayExpress and CPTAC/HPA datasets. Multi-omics profiling identified RPLP0 as a prognostic biomarker linked to patient outcomes and immunotherapy response, with its expression tied to features of the tumor immune microenvironment. These findings suggest RPLP0 could be clinically useful for risk stratification and for predicting benefit from immunotherapy in ccRCC.

Wang B, Liu H, Guo Y et al. · BMC cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Spatial architecture of tertiary lymphoid structures represents an independent prognostic dimension in hepatocellular carcinoma.

This study examined hepatocellular carcinoma (HCC) tissue architecture by developing SpatialDecoder, a deep learning pipeline that segments tertiary lymphoid structures (TLS), classifies TLS maturation subtypes, and assigns spatial compartments (intratumoral, peritumoral, capsular). It found that the spatial architecture of TLS provides an independent prognostic dimension, with anatomical context and maturation subtype contributing to outcome stratification. These results suggest that spatially resolved TLS features could improve prognostic modeling and guide immunotherapy-relevant patient selection in HCC.

Liu W, Zhu C, Cui Z et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Single-cell and spatial omics reveals region-specific plasticity and therapeutic vulnerabilities in metastatic high-risk neuroblastoma.

This study used single-cell and spatial multiomics to characterize cellular heterogeneity and therapeutic vulnerabilities in metastatic high-risk neuroblastoma, comparing lymph node metastases to primary adrenal tumors. It found that metastases exhibit distinct plasticity with mesenchymal-like and stem-like states and increased epithelial-to-mesenchymal transition activity, along with an immunosuppressive myeloid-enriched metastatic niche. These data identify region-specific metastatic states and vulnerabilities that could inform targeted therapies for high-risk neuroblastoma patients.

Wu LMN, Oblinger JL, Xin D et al. · Science advances · (2026) · View on PubMed ↗

Remodeling of the tumor microenvironment in muscle-invasive bladder cancer: insights from single-cell and spatial transcriptomics after neoadjuvant immunochemotherapy.

This study examined how neoadjuvant immunochemotherapy—PD-L1 blockade plus cisplatin-based chemotherapy—remodels the tumor immune microenvironment in muscle-invasive bladder cancer (MIBC) patients, comparing RECIST 1.1 radiologic responders versus non-responders using single-cell and spatial transcriptomics. The authors report that specific immune cell subsets, intercellular communication networks, and their spatial distributions within the tumor microenvironment differ between response groups, identifying features linked to nICT sensitivity and resistance. These findings support spatially resolved immune profiling as a strategy for predicting and improving response to PD-L1/cisplatin neoadjuvant therapy in MIBC.

Zhao G, Bai Y, Chen X et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Circulating immune profiling reveals impaired monocyte states and trajectories driving immunosuppression in glioblastoma.

This study used multimodal single-cell profiling of peripheral blood mononuclear cells from treatment-naïve glioblastoma (GBM) patients and healthy donors, integrating mass/flow cytometry with single-cell RNA-sequencing plus pseudo-temporal trajectory and cell-cell communication inference. The authors found impaired monocyte states and trajectories in GBM that drive systemic immunosuppression. Scientifically, mapping these circulating monocyte programs may yield diagnostic biomarkers and therapeutic targets to counter peripheral immune dysfunction in GBM.

Scafidi A, Kaoma T, Cerella C et al. · Journal of neuroinflammation · (2026) · View on PubMed ↗ · Free PDF ↗

Rbm5 sustains leukemia stem cells through a Myc-driven transcriptional circuitry.

This mechanistic study investigated how the RNA-binding protein Rbm5 regulates leukemia stem cells (LSCs) in acute myeloid leukemia using murine leukemogenesis models. Rbm5 was shown to selectively promote murine leukemogenesis, maintain LSC self-renewal in vivo, and drive LSC gene expression via a Myc-driven transcriptional circuitry, with Rbm5 deficiency impairing self-renewal genes and inducing myeloid differentiation. These findings identify Rbm5–Myc transcriptional control as a potential therapeutic vulnerability to target AML LSCs.

Zhang M, Fields S, Zhang Q et al. · Leukemia · (2026) · View on PubMed ↗ · Free PDF ↗

Genomic landscape of rare variants in a Chinese autism cohort and discovery of novel risk genes.

This whole-genome sequencing study analyzed 3109 samples from 1033 Chinese autism spectrum disorder (ASD) families to define the genomic landscape of rare variants and discover risk genes in an East Asian cohort. Rare ASD-associated variants were identified in 19.2% of affected individuals, with enrichment of de novo variants in probands and nomination/strengthening of candidate genes such as NCL, SPPL3, ADGRB1, and SLC9A3. The population-specific results improve understanding of ASD genetic architecture in Chinese families and expand the catalog of rare-variant risk genes.

Tan S, Lyu Y, Sun X et al. · Molecular psychiatry · (2026) · View on PubMed ↗

Missense but mis-spliced: germline TP53 variant c.671A > C (p.E224A) and the path from uncertainty to pathogenicity.

This study investigated the germline TP53 variant c.671A>C (p.E224A) in a 2-year-old child with retroperitoneal rhabdomyosarcoma and a family history consistent with Li-Fraumeni syndrome, using functional assays in yeast and human cells. Although the variant is predicted to be a missense change, the work showed evidence of mis-splicing and used functional testing to support pathogenicity along the “uncertainty to pathogenicity” pathway. Scientifically, it underscores how combined genetic context and functional splicing assays can reclassify TP53 variants for improved hereditary cancer risk assessment.

Velkova I, Cappato S, Rivera D et al. · Scientific reports · (2026) · View on PubMed ↗ · Free PDF ↗

Long-read sequencing of single cell-derived melanoma sublines reveals divergent and parallel genomic and epigenomic evolutionary trajectories.

This study introduced a long-read sequencing approach for genomic and epigenomic profiling of single-cell-derived melanoma sublines to capture SNVs, structural variants, and DNA methylation changes across evolutionary stages. Using this method, the authors profiled 23 sublines from a mouse cutaneous melanoma cell line and identified divergent and parallel evolutionary trajectories in both genome and epigenome. Scientifically, it demonstrates that long-read single-cell subline sequencing can better resolve tumor evolution mechanisms that are difficult to capture with short-read technologies.

Liu Y, Goretsky A, Keskus AG et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer microenvironment: fibroblasts, stromal signaling, and immune suppression

The CAFs-derived YAP1-periostin axis forms a fibrotic tumor microenvironment to promote metastatic lung tumor growth.

This study examined how cancer-associated fibroblasts (CAFs) regulate metastatic lung tumor growth via a YAP1–periostin axis, focusing on the CD248–periostin–integrin β1 (ITGB1) signaling pathway in non-small cell lung cancer (NSCLC). Using RNA sequencing, immunohistochemistry, coculture assays, and genetic mouse models, the key finding was that CD248+ CAFs promote NSCLC metastasis by driving periostin/ITGB1-mediated fibrotic tumor microenvironment formation. Scientifically, it delineates a CAF-derived pro-metastatic signaling circuit, and clinically it suggests CD248/periostin/ITGB1 as potential therapeutic targets to limit NSCLC metastatic progression.

Wu J, Wang X, Yang Z et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Stromal BMP signalling maintains stem cell genome integrity and prevents gastric cancer initiation.

This study analyzed single-cell RNA-seq data and performed genetic disruption of bone morphogenetic protein (BMP) signaling in Col1a2+ stromal cells or Acta2+ myocytes/pericytes to determine how stromal BMP signaling affects gastric stem cell genome integrity and cancer initiation. Suppressed BMP signaling in stromal cells, but not in gastric stem cells themselves, led to mutations in gastric stem cells and triggered gastric cancer initiation. These findings identify stromal BMP signaling as a niche-protective pathway that maintains stem cell genomic stability and could be targeted to prevent gastric cancer.

Li Z, Wang Z, Yang R et al. · Cell death & disease · (2026) · View on PubMed ↗ · Free PDF ↗

Fibroblast-specific ablation of MHC-I antigen presentation via the IGF2 axis cripples CD8+ T cell surveillance in lung cancer.

This study investigated how cancer-associated fibroblasts (CAFs) regulate CD8+ T cell dysfunction in human non–small cell lung cancer (NSCLC) by focusing on the insulin-like growth factor 2 (IGF2) axis and major histocompatibility complex class I (MHC-I) antigen presentation. Single-cell analysis of 84 human NSCLC samples identified IGF2+ CAFs as a key immunosuppressive subset, and fibroblast-specific IGF2 knockout increased MHC-I antigen presentation cell-autonomously, enhancing CD8+ T cell effector function and improving tumor control and synergy with PD-1 blockade. Scientifically and therapeutically, targeting the fibroblast IGF2→MYC→DNMT1→STAT1 methylation pathway may restore antigen presentation and strengthen checkpoint inhibitor responses in lung cancer.

Song D, Li X, Xiao Q et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

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Cell therapy and immunotherapy engineering (CAR-T, vaccines, co-stimulation)

Injectable bioinstructive microfoam for rapid bedside/in vivo programming of CAR-T cells.

This preclinical/early translational study developed a methylcellulose-based injectable bioinstructive microfoam to rapidly program chimeric antigen receptor (CAR) T cells for subcutaneous administration after blood collection. The key finding was that colocalizing T cells and the CAR vector within the microfoam enabled efficient CAR gene transfer and rapid generation of functional CAR-T cells that then dispersed systemically and mediated regression of distal tumors in vivo. This is significant because it offers a faster, potentially lower-cost CAR-T manufacturing workflow that could improve access and reduce treatment delays for hematologic malignancies and solid tumor exploration.

Stephan SB, Cummings CL, Fitzgerald K et al. · Molecular therapy : the journal of the American Society of Gene Therapy · (2026) · View on PubMed ↗ · Free PDF ↗

A distinct antigen presentation pathway drives potent T cell immunity in lipid nanoparticle-based mRNA vaccines.

This study examined the cellular mechanism by which lipid nanoparticle (LNP)–encapsulated mRNA vaccines drive unusually potent antigen-specific cytotoxic CD8 T cell responses in mice. It found that mRNA-LNP induces long-lasting CD8 T cell expansion through a distinct antigen presentation pathway that differs from conventional adjuvant strategies, yielding about an order of magnitude more antigen-specific CD8 T cells than antigen plus immunostimulants such as lipopolysaccharide or polyinosinic acid. These findings provide mechanistic guidance for designing next-generation mRNA-LNP vaccines that optimize CD8 T cell immunity via antigen presentation routes rather than relying solely on classical adjuvants.

Muro R, Wang S, Ito-Kureha T et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Anti-CAR Immunity Drives Acquired Therapeutic Resistance to GD2-CAR T Cell Therapy in Diffuse Midline Glioma.

This preprint study investigated mechanisms of acquired resistance to GD2-CAR T cell therapy in H3K27M+ diffuse midline glioma (DMG) by analyzing cerebrospinal fluid (CSF) lymphocytes longitudinally. Using single-cell RNA sequencing and TCR sequencing in patients receiving intravenous followed by sequential intracerebral GD2-CAR therapy (with lymphodepleting chemotherapy once prior to CAR T start; NCT04196413), it found that anti-CAR immunity limited GD2-CAR T cell persistence and clonal expansion while non-engineered CSF lymphocytes expanded. Scientifically, it identifies anti-CAR immune responses as a driver of therapeutic resistance, informing strategies to improve CAR T durability in DMG.

Chen Y, Reynolds K, Koch MRA et al. · medRxiv : the preprint server for health sciences · (2026) · View on PubMed ↗ · Free PDF ↗

Dietary restriction is evolutionary conserved on the phenotypic and mechanistic level.

This study tested whether dietary restriction (DR) is conserved across evolution by measuring longevity and fecundity responses to DR in eight Drosophila species and then performing comparative transcriptomics. The key finding is that DR shows overall phenotypic conservation and strongly concordant gene expression responses across species, while evolutionary analysis suggests many top DR-responsive orthologs are “young” genes. Scientifically, this supports a conserved DR response at the phenotypic and transcriptomic levels while indicating that the genetic basis may be more lineage- or time-dependent than previously assumed.

Gautrey SL, Dunning LT, Gossmann TI et al. · EMBO reports · (2026) · 3 citations · View on PubMed ↗ · Free PDF ↗

Englumafusp alfa plus glofitamab in B cell non-Hodgkin lymphoma: a phase 1 trial.

This phase 1 open-label trial evaluated englumafusp alfa (a CD19-4-1BBL co-stimulatory molecule) plus glofitamab in patients with relapsed or refractory aggressive B-cell non-Hodgkin lymphoma, with obinutuzumab pretreatment given 7 days before the first glofitamab dose. The study tested escalating doses of englumafusp alfa alongside a glofitamab step-up dosing schedule followed by repeated cycles of the combination. Clinically, it targets an off-the-shelf immunotherapy strategy by pairing CD19-directed T-cell activation (glofitamab) with 4-1BBL co-stimulation (englumafusp alfa) to improve outcomes in R/R B-NHL.

Hutchings M, Dickinson M, Gritti G et al. · Nature medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Cardiometabolic risk, vascular disease, and metabolic biomarker trajectories

Factors associated with pharmacologic serum concentration of magnesium and corresponding obstetric outcomes among women with severe preeclampsia at Iringa regional referral hospital.

This analytical cross-sectional study at Iringa regional referral hospital evaluated factors affecting pharmacologic serum magnesium concentrations in women with severe preeclampsia receiving magnesium sulphate (MgSO4) and related these levels to obstetric outcomes. The key finding was that magnesium serum concentration after MgSO4 initiation varied according to patient/clinical factors and that magnesium levels were associated with obstetric outcomes, highlighting the need for monitoring to balance efficacy and toxicity. Clinically, the results support serum magnesium level surveillance and dose/administration optimization to improve seizure-prevention effectiveness while reducing the risk of MgSO4-related adverse effects in severe preeclampsia.

Kileo JS, Matovelo S, Kitinusa G et al. · BMC pregnancy and childbirth · (2026) · View on PubMed ↗

Advances in Traditional Chinese Medicine for Diabetic Glaucoma: A Systematic Review From Holistic Pathogenesis to Multi-Target Interventions.

This systematic review synthesized evidence on Traditional Chinese Medicine (TCM) approaches for diabetic glaucoma, focusing on holistic pathogenesis and multi-target interventions in the context of diabetic retinal injury. The key finding was that TCM strategies—framed by syndrome differentiation—are reported to target multiple disease mechanisms beyond intraocular pressure control, including oxidative stress, inflammation, microcirculatory dysfunction, and retinal ganglion cell (RGC) apoptosis. Scientifically and clinically, the review supports further rigorous trials to validate TCM multi-target neuroprotective effects and to clarify which interventions best delay diabetic glaucoma progression.

Liu J, Yu Y, Hu C et al. · Medicinal research reviews · (2026) · View on PubMed ↗

Coffee as a polypharmacological modulator of mitochondrial health: from molecular mechanisms to translational implications.

This narrative review examined coffee as a polypharmacological modulator of mitochondrial health, integrating evidence for multiple coffee-derived bioactives (e.g., chlorogenic acids, trigonelline, diterpenes, melanoidins) rather than caffeine alone. The key finding was a proposed mechanistic framework in which these compounds act synergistically as a systemic “mitochondrial network optimizer,” influencing mitochondrial function and thereby contributing to chronic disease prevention. Translationally, the review motivates more targeted mechanistic studies and biomarker-driven clinical research to determine which coffee constituents and mitochondrial pathways are most relevant for cardiovascular and metabolic outcomes.

Jiang Z, Ding Y · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Chronic obstructive pulmonary disease and risk of digestive diseases: observational and mendelian randomization analyses in the China Kadoorie Biobank.

This observational and Mendelian randomization analysis used the China Kadoorie Biobank to assess whether chronic obstructive pulmonary disease (COPD) is associated with risk of incident digestive diseases in a Chinese population. The key finding was that COPD and/or airflow obstruction severity showed measurable associations with subsequent digestive disease risk, with Mendelian randomization used to evaluate potential causal relationships. The significance lies in clarifying COPD–digestive comorbidity risk and informing prevention strategies and causal inference for shared pathophysiology in large-scale populations.

Zhao Y, Ke Y, Sun D et al. · Respiratory research · (2026) · View on PubMed ↗ · Free PDF ↗

Associations of cumulative exposure and dynamic trajectories of the cholesterol-HDL-glucose index and its obesity-related derivatives with cardiovascular disease: a nationwide prospective cohort study.

This nationwide prospective cohort study evaluated associations between cumulative exposure and longitudinal trajectories of the cholesterol–HDL–glucose index (CHG) and obesity-related derivatives with cardiovascular disease (CVD) risk in CVD-free participants from CHARLS. The key finding was that specific CHG exposure levels and trajectory patterns were associated with differential CVD risk and that some obesity-related derivatives improved discrimination for CVD prediction. This is significant because it supports using dynamic metabolic biomarker trajectories (not just single measurements) to refine CVD risk stratification.

Wang H, Song G, Li G et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

Lipoprotein(a), insulin resistance, and cardiovascular outcomes in metabolic dysfunction-associated steatotic liver disease.

This UK Biobank study assessed whether lipoprotein(a) [Lp(a)] and insulin resistance (IR), measured by the triglyceride-glucose (TyG) index, jointly predict cardiovascular outcomes in adults with metabolic dysfunction-associated steatotic liver disease (MASLD). The key finding was that higher Lp(a) (≥125 nmol/L) and higher IR (TyG index high) were associated with worse cardiovascular outcomes, with evidence for combined risk stratification by Lp(a) and TyG categories. Clinically, the results suggest that integrating Lp(a) and TyG-based IR assessment could improve cardiovascular risk prediction and targeting in MASLD patients.

Dong B, Chen Y, He F et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

Non-steroidal mineralocorticoid receptor antagonists in non-diabetic kidney disease: a narrative review of mechanisms and clinical advances.

This narrative review summarized mechanistic and clinical advances for non-steroidal mineralocorticoid receptor antagonists (ns-MRAs) in non-diabetic kidney disease (NDKD). The key finding was that ns-MRAs protect kidneys through multi-level suppression of mineralocorticoid receptor–driven inflammation and fibrosis, including effects on podocyte injury and progression in both glomerular and tubulointerstitial compartments. Scientifically and clinically, the review supports ns-MRAs as promising therapies for NDKD and highlights mechanistic rationale for their continued development and use.

Luo F, Hu J, Fang H et al. · BMC nephrology · (2026) · View on PubMed ↗ · Free PDF ↗

Extracellular matrix stiffness directs region-specific lung epithelial differentiation revealed by hPSC-derived lung organoids.

This work used human pluripotent stem cell (hPSC)-derived lung organoids embedded in stiffness-tunable hydrogels to test how extracellular matrix (ECM) mechanical stiffness directs region-specific epithelial differentiation along the airway–alveolar axis. Stepwise softening of ECM stiffness produced proximal-to-distal airway epithelial compositions, while increased stiffness during alveolar differentiation promoted maturation of alveolar type 2 (AT2) and type 1 (AT1) cells. The study provides mechanistic evidence that ECM stiffness can instruct lung lineage fate, informing regenerative and disease-modeling strategies.

Liao Z, Meng H, Lv J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Frailty-related plasma proteomic signatures and key biomarkers for new-onset dementia and its subtypes: A prospective cohort study.

This prospective cohort study analyzed frailty-related plasma proteomic signatures in 52,000+ UK Biobank participants without dementia at baseline, using 2,915 plasma proteins and incident dementia ascertainment from hospital and mortality records. Frailty (physical frailty and a 49-item frailty index) was associated with specific proteomic signatures and individual proteins that predicted new-onset dementia and helped characterize dementia subtypes. These findings suggest plasma proteomics can mechanistically link frailty to dementia risk and improve biomarker-based stratification for prevention trials.

Zhang X, Huang Q, Huang J et al. · Journal of advanced research · (2026) · View on PubMed ↗ · Free PDF ↗

Dibromoacetic acid impairs spermatogenesis: integrative evidence from human epidemiology, network toxicology, and mechanistic validation.

Combining human epidemiology with network toxicology and mechanistic validation, this integrative study assessed dibromoacetic acid (DBA) exposure and its effects on male reproductive outcomes in 282 men with urinary DBA measured at near-universal detection. DBA exposure was significantly associated with lower sperm concentration/count, and mechanistic experiments supported disruption of histone-to-protamine replacement during sperm chromatin remodeling. These findings implicate DBA as a modifiable environmental risk factor for impaired spermatogenesis and point to a specific chromatin-remodeling mechanism.

Wang S, Zhang P, Tan X et al. · Environment international · (2026) · View on PubMed ↗ · Free PDF ↗

TRIM72 alleviates skeletal muscle atrophy by modulating mt-dsRNA/RIG-I signaling.

In multiple murine models of muscle atrophy (aging, denervation, and dexamethasone), this study tested how TRIM72 affects mitochondrial double-stranded RNA (mt-dsRNA)/RIG-I signaling to drive wasting. The key finding was that TRIM72 alleviated skeletal muscle atrophy by modulating mt-dsRNA/RIG-I–mediated innate immune activation, linking mitochondrial dsRNA sensing to inflammation and muscle loss. This provides a potential therapeutic target pathway for preventing or treating muscle atrophy across diverse etiologies.

Liao L, Zheng Z, Xu W et al. · Metabolism: clinical and experimental · (2026) · View on PubMed ↗

Characteristics and outcomes of patients with imaging-defined MASLD and histological steatosis grade S0.

This cohort study characterized patients with imaging-defined MASLD who had no steatosis on biopsy (steatosis grade S0) and evaluated outcomes and causes of this discordance. The key finding was that “steatosis 0” represents a clinically meaningful subgroup with identifiable drivers (including fat distribution patterns assessed by MRI-PDFF) and variable histologic progression on paired biopsies. Scientifically and clinically, it highlights limitations of imaging-only MASLD diagnosis and informs how to interpret and manage patients with biopsy-negative steatosis.

Liu WY, Lian LY, Kim SU et al. · The American journal of gastroenterology · (2026) · View on PubMed ↗

Absolute risk of malignancy by treatment in patients with Crohn’s disease compared to the general population: a nationwide population-based cohort study.

Using nationwide Swedish registers in a population-based cohort, this study quantified absolute malignancy risk in 38,733 patients with Crohn’s disease by treatment exposure (thiopurines, TNF inhibitors, combination therapy, vedolizumab, ustekinumab, and immunomodulator-naïve) compared with the general population. The key finding was that cancer incidence differed by treatment class, with absolute risk estimates provided as age-stratified incidence rate differences using a once-exposed-always-exposed design. These results improve real-world patient counseling by translating Crohn’s treatment choices into absolute malignancy risk.

Everhov ÅH, Eriksson J, Söderling J et al. · The American journal of gastroenterology · (2026) · View on PubMed ↗ · Free PDF ↗

Recompensation of decompensated cirrhosis in a spectrum of metabolic-dysfunction-related steatotic liver disease, with PEth-corroborated alcohol abstinence and modification of cardiometabolic risk factors.

This Hepatology study evaluated recompensation of decompensated cirrhosis across metabolic-dysfunction-related steatotic liver disease (MASLD) and MetALD (MASLD with alcohol consumption) using Baveno VII criteria in 344 patients, with interventions including alcohol abstinence, dry weight loss, and cardiometabolic risk modification. The key finding was that a subset of patients achieved recompensation and that modifiable factors—particularly PEth-corroborated alcohol abstinence and cardiometabolic risk management—were associated with improved outcomes. Clinically, it supports that targeted, modifiable management can reverse decompensation in a portion of patients with steatotic liver disease-related cirrhosis.

Premkumar M, Sandhu A, Sharma P et al. · Hepatology (Baltimore, Md.) · (2026) · View on PubMed ↗

Integrated Fat-Muscle Patterns Drive Sex-Specific Diabetes Risk: UK Biobank Evidence.

This UK Biobank study analyzed sex-specific associations between integrated body composition patterns and incident type 2 diabetes (T2D) in 258,500 diabetes-free participants. Using principal component analysis (PCA) on 28 anthropometric and strength traits, followed by LASSO-penalized Cox and weighted quantile sum (WQS) regression, it identified seven interpretable body composition patterns and reported that specific components were consistently associated with T2D risk in a sex-dependent manner over a mean 11-year follow-up. These findings support using multivariate fat–muscle patterning to improve prediction and potentially tailor prevention strategies for T2D by sex.

Ma Y, Zhou N, Yu B et al. · Diabetes · (2026) · View on PubMed ↗ · Free PDF ↗

Persistent tissue hypoperfusion improves risk stratification beyond vasopressor dose in refractory septic shock: a secondary analysis of the ANDROMEDA-SHOCK-2 trial.

This exploratory secondary analysis of the ANDROMEDA-SHOCK-2 trial studied refractory septic shock in adults after 6 hours of protocolized hemodynamic resuscitation, using norepinephrine equivalent dose (NEE) plus persistent tissue hypoperfusion markers (abnormal capillary refill time and non-decreasing lactate). Persistent tissue hypoperfusion—operationalized as NEE >0.5 µg/kg/min together with capillary refill time >3 s and non-decreasing lactate—improved mortality risk stratification beyond vasopressor dose alone. Clinically, this supports adding bedside tissue perfusion measures to define refractory septic shock more accurately than vasopressor escalation criteria by themselves.

Kattan E, Ospina-Tascón GA, Orozco N et al. · Intensive care medicine · (2026) · View on PubMed ↗

Key principles for rehabilitation of critically ill patients with obesity.

This narrative review examined rehabilitation needs of critically ill patients with obesity across the recovery trajectory, synthesizing evidence on how body composition and obesity-related pathophysiology shape outcomes. It identifies three obesity-related survivor phenotypes that may influence rehabilitation response and emphasizes interprofessional, patient-centered strategies tailored to these phenotypes. Scientifically and clinically, the review provides a framework to improve rehabilitation planning and outcomes in ICU survivors with obesity by moving beyond one-size-fits-all approaches.

Eggmann S, Bear DE, Bourne RS et al. · Intensive care medicine · (2026) · View on PubMed ↗ · Free PDF ↗

An integrated experimental and computational systems biology analysis reveals molecular mechanisms underlying reproductive toxicity induced by manganese and atrazine.

This integrated experimental and computational systems biology study investigated combined reproductive toxicity of atrazine (ATZ) and manganese (Mn) in male Wistar rats treated for 28 days, using biochemical assays, oxidative/inflammatory indices, sperm quality measures, and DNA fragmentation alongside in silico analyses. The combined ATZ+Mn exposure produced additive or synergistic disruptions in testicular function and reproductive hormones with increased oxidative/inflammatory stress and DNA fragmentation compared with controls or single exposures. These findings mechanistically link ATZ and Mn toxicity pathways relevant to male fertility and support systems-level risk assessment for co-exposure scenarios.

Owumi S, Chimezie J, Otunla MT et al. · Naunyn-Schmiedeberg’s archives of pharmacology · (2026) · View on PubMed ↗

Evolving utilization of bariatric surgery since the rise of semaglutide and tirzepatide.

This study analyzed nationwide utilization trends in bariatric surgery in the Epic Cosmos database from 2018–2025, focusing on how preoperative semaglutide or tirzepatide (GLP-1 receptor agonists) dispense history relates to surgery use. It reports evolving bariatric surgery utilization patterns coinciding with the rise of semaglutide and tirzepatide and identifies factors associated with pre-surgery GLP-1RA use using modified Poisson regression with hospital- and state-level multilevel modeling. The results are significant for health-system planning and for understanding how pharmacologic obesity treatment is shifting demand for surgical management.

Kozato A, Patel SS, Orandi BJ et al. · Surgical endoscopy · (2026) · View on PubMed ↗

Pharmacological treatment of MASH.

This review article summarized current pharmacological approaches for metabolic dysfunction-associated steatotic liver disease (MASLD), including its progressive inflammatory form MASH, and discussed how these therapies target shared cardiometabolic drivers such as insulin resistance and low-grade inflammation. It emphasizes MASLD’s strong epidemiologic links to type 2 diabetes, cardiovascular disease, chronic kidney disease, and extrahepatic cancers and frames treatment selection around these mechanisms. Scientifically, it consolidates the rationale for drug development and clinical use in a disease spectrum where metabolic comorbidity is central to progression.

Stefan N, Targher G · Diabetologia · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Peripheral artery disease: advances in medical therapy.

This review focused on advances in medical therapy for peripheral artery disease (PAD), addressing underdiagnosis/undertreatment and highlighting strategies targeting metabolic, lipid, immuno-inflammatory, and thrombotic drivers. It synthesizes evidence supporting multifaceted guideline-directed approaches—along with lifestyle interventions such as smoking cessation—to reduce major adverse cardiovascular events (MACE) and major adverse limb events (MALE). Clinically, it provides an updated therapeutic roadmap aimed at improving outcomes by closing gaps between evidence and real-world PAD management.

Garagoli F, Slipczuk L, Shapiro MD et al. · European heart journal · (2026) · View on PubMed ↗ · Free PDF ↗

Emerging insights into inflammation-driven atherosclerosis: immune cell mechanisms.

This review studied immune-cell mechanisms driving inflammation-driven atherosclerosis, focusing on how recruited macrophages, T cells, B cells, dendritic cells, and neutrophils sustain plaque development after endothelial activation. It found that endothelial permeability and leukocyte adhesion enable a self-amplifying immune cascade that promotes vascular constriction and activation of inflammatory pathways leading to atheromatous plaque growth. These integrated immune insights support more targeted anti-inflammatory strategies for preventing or treating atherosclerosis beyond lipid lowering.

Mohamud AO, Dai Z · Frontiers in cardiovascular medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Comparative efficacy of traditional and modern mind-body exercises in middle-aged and older adults with knee osteoarthritis: a network meta-analysis of randomized controlled trials.

This network meta-analysis studied the comparative efficacy of traditional versus modern mind-body exercise interventions in middle-aged and older adults with knee osteoarthritis, using randomized controlled trials and outcomes including WOMAC pain, function, and stiffness plus psychological and physical measures. It found differential effects across mind-body modalities on KOA-related pain, function, stiffness, and secondary outcomes, with relative rankings favoring specific exercise approaches (as synthesized across the included trials). The results help clinicians choose among mind-body exercise options for symptom control in older KOA populations.

Pan R, Mi A, Cheng H · Frontiers in medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Global Trends in the Burden of Ischemic Stroke Attributable to Diabetes Versus Atrial Fibrillation.

This study analyzed global trends in ischemic stroke burden attributable to diabetes versus atrial fibrillation using Global Burden of Disease 2021 data, applying population-attributable fractions and joinpoint regression with projections to 2050. It found distinct temporal and age/location patterns for diabetes-related versus AF-related ischemic stroke burden, indicating different trajectories and preventable proportions by risk factor elimination. These findings clarify where prevention efforts targeting diabetes versus atrial fibrillation may yield the greatest reductions in future ischemic stroke burden.

Wang L, Lin F, Chen Y et al. · Stroke · (2026) · View on PubMed ↗

Pregnancy- and lactation-associated osteoporosis: A position statement of the IAPM, IOF, ECTS, ESCEO, IMS, and EMAS.

This position statement studied pregnancy- and lactation-associated osteoporosis (PLO) by reviewing evidence on its assessment, diagnosis, and treatment, including safety considerations and factors influencing outcomes. It found that PLO is characterized by fragility fractures—most often vertebral and sometimes multiple—occurring in late pregnancy or early postpartum, and it recommends structured clinical evaluation and management despite limited controlled comparative trials due to rarity. The significance is standardized guidance for clinicians to improve diagnosis and treatment decisions for this uncommon but high-risk condition.

Hadji P, Athanasiadis A, Brandi ML et al. · International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · (2026) · View on PubMed ↗ · Free PDF ↗

Comparative effectiveness of mepolizumab and omalizumab in patients eligible for both: a retrospective cohort study.

This retrospective cohort study compared real-world effectiveness of mepolizumab versus omalizumab in asthma patients eligible for both therapies, using eligibility defined by blood eosinophils (≥150 cells/μL or ≥300 cells/μL in the prior year), total IgE (≥30 IU/mL), and sensitization to a perennial inhalant allergen. It found differences in adjusted incidence outcomes between the two biologics in this overlapping-eligibility population, indicating that one therapy may perform better than the other depending on the endpoint used. Clinically, the study supports more evidence-based selection of biologic therapy for severe asthma patients who meet criteria for both anti–IL-5 and anti-IgE treatment pathways.

Nagai T, Inoshima N, Matsui H et al. · Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Platelet homeostasis and heterogeneity in inflammation and sepsis: mechanisms, biological effects, and clinical potential.

This review studied platelet homeostasis and heterogeneity in the context of inflammation and sepsis, focusing on how platelets link hemostasis, immunity, and immunothrombosis. It found that platelets actively modulate immune responses—driving inflammatory amplification and platelet–immune cell interactions—that contribute to organ injury in sepsis. The clinical significance is that platelet-based mechanisms and biomarkers could inform risk stratification and therapeutic targeting in sepsis.

Pan Y, Zhao W, Yu B et al. · Cell communication and signaling : CCS · (2026) · View on PubMed ↗ · Free PDF ↗

Association between the combined cholesterol, high-density lipoprotein, glucose index and frailty index and new-onset cardiovascular disease in individuals with cardiovascular-kidney-metabolic syndrome stages 0-3: evidence from CHARLS.

This CHARLS cohort study evaluated whether a combined cholesterol, high-density lipoprotein, glucose index and frailty index (CHG-FI) predicts new-onset cardiovascular disease outcomes in individuals with cardiovascular-kidney-metabolic syndrome stages 0–3. The key finding is that integrating metabolic dysregulation (cholesterol/HDL/glucose) with frailty (CHG-FI) provides better risk association and predictive utility for incident CVD, heart disease, and stroke than single-domain markers. Clinically, CHG-FI could enable earlier identification of middle-aged and older adults at high risk for cardiovascular events before overt disease develops.

Sun Z, Wang K, Guo C et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

Dietary and supplemental calcium intake and bone changes during antiresorptive osteoporosis treatment in older women: a longitudinal observational study.

This longitudinal observational study in older women receiving antiresorptive osteoporosis treatment tested how dietary calcium and protein intake versus calcium supplementation relate to changes in total hip bone mineral density (BMD) and bone strength. The key finding is that in calcium-replete women, calcium supplements had little additional effect, whereas low protein intake blunted the benefits of antiresorptive therapy. These results suggest that optimizing nutrition (especially protein) may be more important than routine calcium supplementation when dietary calcium is already adequate.

Papageorgiou M, Gugler Y, Ferrari S et al. · Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · (2026) · View on PubMed ↗

Interleukin-18 armours antitumour immune effectors.

This Nature Reviews Immunology article reviews therapeutic strategies that “armour” antitumor immune effectors with interleukin-18 (IL-18), including engineered T-cell approaches designed to enhance adoptive cell therapy and other immunotherapies. The key translational message is that IL-18–based engineering can modulate the tumor microenvironment, but treatment response and resistance depend on molecular mechanisms that must be understood for effective patient selection. The review is significant because it frames IL-18 armouring as a promising next-generation immunotherapy while highlighting mechanistic biomarkers and resistance pathways needed for clinical translation.

Sharma A, Bishara GG, Olejniczak SH et al. · Nature reviews. Immunology · (2026) · View on PubMed ↗

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Generated automatically on July 19, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.