PubMed Trending Research Digest — July 05, 2026

Automated digest · 99 articles · 15 research areas · July 05, 2026

Overview

Across this week’s papers, a dominant theme is precision stratification—using molecular signatures, imaging frameworks, and standardized criteria—to improve who benefits from therapy and how outcomes are measured. Examples include proteomic and ctDNA MRD biomarker work in ALS and colorectal liver metastases, foundation-model approaches for immunotherapy prediction across cancers, and consensus frameworks for PET response assessment in neuroendocrine tumors and diagnostic standardization in advanced prostate cancer. In parallel, multiple studies emphasize that real-world implementation and context (e.g., guideline adherence in primary hyperoxaluria, information conditions for LLM triage, and baseline antibiotic/PPI exposure affecting immunotherapy outcomes) can strongly shape clinical performance.

A second major thread is immune modulation—both mechanistically and therapeutically. Cancer immunotherapy papers span CAR-T/NK engineering to overcome exhaustion and tumor microenvironment suppression, metabolic checkpoints that regulate immune evasion (e.g., SOAT1/ACAT1 in HCC), and innate immune pathways that influence systemic responses to radiotherapy (Gal-9/TIM-3). Outside oncology, studies highlight immune aging and inflammation as causal biology (STING-driven peripheral inflammation in Parkinson’s risk, immune aging biomarker frameworks, PD-1 pathway control of pathogenic T cells in rheumatoid arthritis) and show how physical and biochemical cues (tissue stiffness, mechanotransduction, complement receptor signaling) can reprogram immune function.

Finally, several studies connect metabolism, inflammation, and neurodegeneration to actionable targets. Work on mitochondrial dysfunction and redox control (in depression and Parkinson’s disease), lysosomal/autophagy defects modeled in patient iPSC systems, and metabolite-driven post-translational regulation (lysine pyruvylation) all point to converging pathways where metabolic state shapes immune signaling and cell fate. In cardiometabolic and cardiovascular domains, trials and observational analyses explore how GLP-1/GIP and other metabolic interventions may reduce downstream risk (including MASLD and postoperative HCC recurrence), while critical-care and renal-inflammation studies refine timing and supportive strategies to improve organ outcomes.

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Neurodegeneration & Neuroinflammation (ALS, PD, Alzheimer’s, MS)

A PARK9 iPSC-Derived Dopaminergic Neuron Model Enables Drug Screening Targeting Autophagy-Lysosome Pathway Dysfunction in Parkinson’s Disease.

This study generated PARK9 patient-derived induced pluripotent stem cells (iPSCs) carrying an ATP13A2 mutation and mutation-corrected isogenic controls to model dopaminergic neurons and test drug screening approaches targeting the autophagy–lysosome pathway in Parkinson’s disease. PARK9 iPSC-derived neurons showed lysosomal dysfunction with impaired lysosomal acidification and reduced mature cathepsin D, recapitulating autophagy-lysosome pathway defects relevant to PD. The iPSC model provides a human, mutation-specific platform for identifying disease-modifying compounds that restore lysosomal/autophagic function in PD.

Tsukiboshi KI, Ishikawa KI, Yamaguchi A et al. · Journal of neurochemistry · (2026) · View on PubMed ↗

Vitamin B6 produced by gut microbiome regulates host behavioral phenotypes through dopaminergic metabolism.

This study examined how gut microbiome-derived vitamin B6 (VB6) and its biosynthesis gene regulate host behavioral phenotypes via dopaminergic metabolism, combining metagenomic analyses of Parkinson’s disease (PD) patient fecal samples with E. coli–C. elegans symbiotic models. The authors found enrichment of VB6/PLP biosynthetic pathways and tyrosine decarboxylase genes in PD microbiomes, and demonstrated that the bacterial pdxJ gene (key for de novo VB6 synthesis) is required to regulate host dopaminergic homeostasis. These results link a specific microbial gene (pdxJ) and metabolite (VB6/PLP) to dopaminergic regulation, suggesting microbiome-targeted strategies for PD-related neurochemical dysfunction.

Kim D, Li M, Nguyen TH et al. · Gut microbes · (2026) · View on PubMed ↗ · Free PDF ↗

Regional mapping of CSF1R-positive microglia in neurodegenerative diseases and progressive MS, with exploratory presynaptic marker analyses.

This study used RNAscope to quantify CSF1R mRNA–positive microglia across six cortical regions in early-onset Alzheimer’s disease (EOAD), late-onset Alzheimer’s disease (LOAD), and progressive multiple sclerosis (MS) lesions, with exploratory comparisons to presynaptic marker burden. The goal was to build a cross-disease, multi-region quantitative map of CSF1R-positive microglia to improve interpretation of CSF1R-PET signals. A region-specific atlas of CSF1R-positive microglia could strengthen patient stratification and biomarker interpretation for CSF1R-targeted therapies and imaging.

Bavarsad MS, Pereira FL, Reinhardt MM et al. · Journal of neuroinflammation · (2026) · View on PubMed ↗ · Free PDF ↗

Mitochondrial-inflammation crosstalk in major depressive disorder: molecular mechanisms and therapeutic implications.

The study reviewed and synthesized evidence on mitochondrial–inflammation crosstalk in major depressive disorder (MDD), focusing on mitochondrial DNA abnormalities, bioenergetic defects, quality control disruption, and redox imbalance. It concluded that mitochondrial damage-associated molecular patterns and excessive reactive oxygen species activate innate immune signaling, while inflammatory challenges further impair mitochondrial integrity, forming a bidirectional self-reinforcing loop. This mechanistic model supports therapeutic strategies that target mitochondrial dysfunction and neuroinflammation in MDD.

Wang Y, Li JT, Zhu LL et al. · Molecular psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗

Therapeutic targeting of the conserved region within the low-complexity domain of TDP-43 is neuroprotective and extends survival in amyotrophic lateral sclerosis mice.

The study tested whether targeting a conserved α-helical region (residues 320–340) within the low-complexity domain of TDP-43 is neuroprotective in amyotrophic lateral sclerosis (ALS) mouse models, using CR deletion and structure-based virtual screening to identify a small molecule. Deleting the conserved region markedly suppressed TDP-43-induced neuronal death, and the brain-penetrant small molecule XL20 was reported to engage this region and confer neuroprotection with survival extension. This supports the conserved TDP-43 region as a druggable target and provides a therapeutic lead for TDP-43–driven neurotoxicity.

Gao J, Shukla D, Ding M et al. · Nature aging · (2026) · View on PubMed ↗ · Free PDF ↗

Global epidemiology of amyotrophic lateral sclerosis: a systematic review and meta-analysis.

This systematic review and meta-analysis synthesized global epidemiology of amyotrophic lateral sclerosis (ALS) by pooling incidence, prevalence, and mortality estimates from studies in the general population. Across 142 included studies, the authors reported a global pooled incidence of 1.65 per 100,000 person-years (with further subgroup results truncated in abstract). The updated global burden estimates are important for health planning and for benchmarking future interventions and research priorities.

Liu RY, Su WM, Duan QQ et al. · Journal of neurology, neurosurgery, and psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗

Inhibiting 15-PGDH restores redox homeostasis and confers neuroprotection in Parkinson’s disease.

This preclinical study examined whether inhibiting 15-hydroxyprostaglandin dehydrogenase (15-PGDH) can restore redox homeostasis and provide neuroprotection in Parkinson’s disease (PD) using PD patient data and multiple mouse models. Pharmacologic 15-PGDH blockade or partial genetic reduction restored redox balance and mitigated microglial and astrocyte activation, dopaminergic neuron loss, and motor impairment across three PD models (systemic MPTP, intranigral LPS, and intrastriatal AAV-α-synuclein). The findings are significant because they identify 15-PGDH inhibition as a potential disease-modifying therapeutic strategy targeting redox dysregulation in PD.

Kim YK, Cha YJ, Park SE et al. · Redox biology · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting astrocytic Dp71 attenuates BBB disruption after traumatic brain injury through WTAP-associated m6A regulation of MMP2.

This study examined how astrocytic dystrophin protein 71 (Dp71) influences blood-brain barrier (BBB) integrity after traumatic brain injury (TBI) in both human samples and mouse models. Down-regulating astrocytic Dp71 reduced secondary BBB disruption, decreased astrocyte activation and inflammatory infiltration, and lowered matrix metalloproteinase-2 (MMP2) release, with the mechanism linked to WTAP-associated m6A regulation of MMP2. The significance is that targeting astrocytic Dp71–WTAP–m6A–MMP2 signaling may offer a therapeutic approach to limit BBB breakdown and secondary injury after TBI.

Wang J, Zhao C, Liu B et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Distinct contributions of two subpopulations of subthalamic neurons to levodopa-induced dyskinesia.

This work investigated, in a mouse model of levodopa-induced dyskinesia (LID), how two subpopulations of subthalamic nucleus (STN) neurons with distinct projection targets regulate dyskinesia versus hypokinesia. STN neurons projecting to the entopeduncular nucleus (EP) showed a U-shaped activation pattern and EP activation alleviated dyskinesia but worsened hypokinesia, whereas STN neurons projecting to the tegmental reticular nucleus (RtTg) produced predominantly inhibitory responses. The results pinpoint projection-specific STN circuitry as a mechanistic basis for refining STN deep-brain stimulation strategies to reduce LID without exacerbating parkinsonism.

Shen B, Han L, Xiao Y et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

STING-dependent peripheral inflammaging drives neurodegeneration via extracellular vesicles.

This study analyzed peripheral inflammaging in the context of Parkinson’s disease risk by combining data from PD patients and LRRK2 gain-of-function (LRRK2GoF) mice, testing a STING-dependent mechanism. It found that STING-dependent peripheral inflammation acts as an accelerated aging driver that contributes to neurodegeneration via extracellular vesicles. The work links a defined innate-immune pathway (STING) to PD-associated accelerated aging biology, suggesting extracellular vesicle–mediated inflammation as a potential therapeutic axis.

Öberg M, Myers C, Saffarzadeh N et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

Non-canonical amino acid incorporation enables minimally disruptive labeling of stress granule and TDP-43 proteinopathy.

This eLife study developed a minimally disruptive protein-labeling method using genetic code expansion to incorporate the fluorescent non-canonical amino acid Anap into G3BP1 (G3BP Stress Granule Assembly Factor 1) and TDP-43 in live cells and neurons. The key finding was that Anap incorporation preserved protein structure/function and faithfully recapitulated stress granule and TDP-43 proteinopathy localization and dynamics, outperforming conventional fluorescent tags. This technique enables more physiologically relevant visualization of ALS-linked TDP-43 and stress granule biology for mechanistic studies and therapeutic target validation.

Chen H, Wang H, Lu YN et al. · eLife · (2026) · View on PubMed ↗ · Free PDF ↗

Exercise and fluoxetine in Alzheimer’s disease: Molecular mechanisms of synergistic and antagonistic effects (Review).

This review synthesized molecular evidence on how exercise may synergize with or counteract the effects of the antidepressant fluoxetine in Alzheimer’s disease (AD). It links exercise-driven improvements in mitochondrial function, antioxidant defenses, neuroinflammation suppression, and synaptic plasticity to neurotrophic signaling and cerebrovascular regulation, while discussing how fluoxetine’s mechanisms could interact with these pathways in ways that may be beneficial or potentially antagonistic. The work supports further mechanistic and translational studies of combined lifestyle and pharmacologic strategies to modify AD pathology and cognitive decline.

Wu M, Li Y · International journal of molecular medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Research advances and application prospects of CAR-T therapy in the treatment of age-related diseases.

This narrative review discussed how chimeric antigen receptor T-cell (CAR-T) therapy could be applied to age-related diseases by targeting mechanisms linked to cellular senescence and the senescence-associated secretory phenotype (SASP). It summarizes molecular pathways of cellular senescence and how chronic inflammatory microenvironments contribute to age-related pathology, then outlines CAR-T’s potential for targeted elimination of pathogenic cells. The review positions CAR-T as a promising platform for future interventions in age-related disorders, while emphasizing the need for systematic development and validation.

An X, Wu T, Gou R et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Immunotherapy & Cellular Therapies (CAR-T/NK/ICI)

Linperlisib enhances MUC1-Tn CAR T cell efficacy by inhibiting EGR1/DUSP2 axis to prevent CAR T cell exhaustion.

The study tested whether linperlisib (a PI3Kδ inhibitor) can enhance MUC1-Tn–targeted CAR T cell efficacy in T-cell acute lymphoblastic leukemia (T-ALL) by preventing exhaustion. Linperlisib improved CAR T cell cytotoxicity in vitro and in xenograft models and mechanistically inhibited the EGR1/DUSP2 axis to reduce CAR T cell exhaustion. These findings support PI3Kδ-pathway modulation as a strategy to improve CAR T durability against MUC1-Tn–positive malignancies.

Wei JY, Liu ZW, Lu QS et al. · Leukemia · (2026) · View on PubMed ↗ · Free PDF ↗

CD7 chimeric antigen receptor T cells in patients with relapsed or refractory CD7-positive acute myeloid leukemia.

This phase I clinical trial evaluated CD7-targeted CAR T cells in patients with relapsed or refractory CD7-positive acute myeloid leukemia (AML). In 14 enrolled patients receiving a single infusion of autologous or donor-derived CD7 CAR T cells with 3+3 dose escalation, the primary endpoint was dose-limiting toxicity and treatment-related adverse events included cytokine release syndrome. The study provides early safety and feasibility evidence for CD7 CAR T therapy in a CD7-expressing AML subset (~30%).

Zhang M, Liu L, Fu S et al. · Leukemia · (2026) · View on PubMed ↗

Neoadjuvant tislelizumab (anti-PD-1 antibody) plus chemotherapy in patients with advanced epithelial ovarian cancer: the exploratory NAIVE trial.

The study evaluated neoadjuvant immunochemotherapy by comparing platinum-based chemotherapy plus the anti–PD-1 antibody tislelizumab (NACI) versus chemotherapy alone (NAC) in patients with FIGO IIIC–IV epithelial ovarian cancer in the exploratory NAIVE phase II trial. The trial assessed 1-year progression-free survival as the primary endpoint and measured immune modulation, R0 resection, response rates, and safety as secondary endpoints. If effective, this regimen could improve outcomes and clarify how adding tislelizumab reshapes antitumor immunity in advanced EOC.

Zhang Z, Fei J, Lao S et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Galectin-9-driven immune evasion constrains radiotherapy-induced systemic antitumor immunity.

This preclinical study investigated how radiotherapy (RT) regulates galectin-9 (Gal-9) and how Gal-9 blockade affects systemic antitumor immunity in tumor-bearing models, focusing on the TIM-3 immune checkpoint axis. RT-induced Gal-9 upregulation promoted immune evasion and constrained RT’s systemic (abscopal) antitumor effects, while combinatorial RT plus Gal-9 blockade enhanced systemic antitumor immune responses. These findings support Gal-9/TIM-3 pathway targeting as a strategy to improve the immunologic reach of RT beyond the irradiated lesion.

Song J, Liu B, Hsieh RC et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Circumventing Ewing sarcoma tumor microenvironment resistance by IL1RAP CAR-modified TGFβ1-imprinted natural killer cells in combination with IL-15 agonist and anti-GD2 antibody.

This study evaluated a combinatorial immunotherapy for metastatic/relapsed/refractory Ewing sarcoma (ES) by engineering IL1RAP CAR-modified natural killer (NK) cells with TGFβ1-imprinting, then combining them with the IL-15 agonist and the anti-GD2 antibody dinutuximab. The approach overcame ES tumor microenvironment–mediated NK immunosuppression by countering TGFβ-driven resistance, while IL1RAP CAR targeting increased tumor-specific killing and dinutuximab enhanced NK ADCC. Clinically, this provides a rationale for multi-pronged CAR-NK plus cytokine agonism and anti-GD2 antibody therapy to overcome TME resistance in ES.

Luo W, Zhang HF, Li W et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Antibody-drug conjugates beyond HER2: Translating evidence into practice for HR+ HER2-negative and triple-negative metastatic breast cancer.

This narrative evidence-to-practice review synthesized clinical data on antibody-drug conjugates (ADCs) beyond HER2 for metastatic breast cancer, focusing on HR+ HER2-negative and triple-negative disease. It highlights expanding roles for trastuzumab deruxtecan, sacituzumab govitecan, datopotamab deruxtecan, and sacituzumab tirumotecan, while emphasizing key implementation challenges including ADC toxicity management, optimal sequencing, and biomarker refinement. The clinical significance is that it provides a practical framework for integrating these ADCs into treatment pathways while improving patient selection and minimizing adverse effects.

Gouveia MC, Freire PJG, Prado CGS et al. · Breast (Edinburgh, Scotland) · (2026) · View on PubMed ↗ · Free PDF ↗

Maintenance therapy in gynecologic malignancies: Current and future state.

This narrative review summarized current and emerging evidence for maintenance therapy in gynecologic malignancies, focusing on strategies after initial chemotherapy to reduce recurrence and prolong progression-free and overall survival. It highlights that continuation maintenance approaches—particularly those using VEGF-targeting agents and PARP inhibitors—have improved progression-free survival in selected settings. The review frames maintenance therapy as a key evolving strategy for patients with advanced disease who remain at high risk of recurrence.

Widick PC, Wright AA, Liu JF · Cancer · (2026) · View on PubMed ↗

Idecabtagene vicleucel and endogenous T-cell phenotypes linked to progression-free survival in relapsed multiple myeloma.

This study analyzed immune dynamics using multidimensional computational flow cytometry in bone marrow aspirates from 107 relapsed multiple myeloma patients treated with the CAR T-cell therapy idecabtagene vicleucel in the KarMMa trial. It found that at screening, longer progression-free survival (PFS) was associated with higher PD1+ cytotoxic T-cell percentages and ICOS-TIGIT+ regulatory T cells, and that early post-infusion CAR-T features (e.g., >1% CAR-T cells and a CD4/CD8 CAR-T-cell ratio >0.09) related to outcomes. These findings are significant for using T-cell phenotype biomarkers to stratify patients and potentially personalize CAR-T therapy in multiple myeloma.

Paiva B, Manrique I, Thompson E et al. · HemaSphere · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Biomarkers, Omics & Computational Oncology

Generalizable AI predicts immunotherapy outcomes across cancers and treatments.

The study developed and evaluated COMPASS, a pan-cancer foundation model that predicts immunotherapy outcomes from bulk tumor transcriptomes across cancers and multiple immune checkpoint inhibitor (ICI) treatments. COMPASS used a concept bottleneck transformer with 44 immune concepts and achieved improved average performance over 22 comparator methods across 16 clinical cohorts spanning seven cancers and six ICIs. This provides a generalizable, transcriptome-based biomarker framework that could guide patient selection for ICIs more reliably across tumor types and therapies.

Shen W, Moon I, Nguyen TH et al. · Nature medicine · (2026) · View on PubMed ↗

Differential impact of proton pump inhibitors and antibiotics on immunotherapy efficacy after chemoradiotherapy in locally advanced non-small-cell lung cancer: a post-hoc analysis of the PACIFIC trial.

This post-hoc analysis of the randomized, double-blind, placebo-controlled PACIFIC phase 3 trial assessed whether baseline proton pump inhibitor (PPI) and antibiotic exposure affects progression-free survival and overall survival in unresectable stage III squamous or non-squamous non-small-cell lung cancer (NSCLC) receiving chemoradiotherapy followed by immunotherapy. Baseline antibiotics and PPIs were associated with worse survival outcomes, supporting the hypothesis that gut microbiome disruption may reduce immune checkpoint inhibitor efficacy even in earlier-stage, locally advanced disease. These findings are clinically significant because they suggest that minimizing unnecessary antibiotics and PPIs around chemoradiotherapy/immunotherapy could improve outcomes for stage III NSCLC patients.

Brunetti L, Santo V, Pinato DJ et al. · The Lancet. Oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Circulating Tumor DNA Status and Adjuvant Chemotherapy in Resected Colorectal Liver Metastases.

This prospective analysis within the CIRCULATE-Japan GALAXY study evaluated whether ctDNA-defined molecular residual disease (MRD) after resection of colorectal liver metastases predicts survival outcomes and modifies benefit from adjuvant chemotherapy. The key finding was that ctDNA MRD status was associated with survival and could stratify patients regarding the effectiveness of adjuvant chemotherapy after curative surgery. Scientifically and clinically, ctDNA MRD may enable more precise selection of patients for adjuvant chemotherapy in resected CRLM.

Kataoka K, Ito K, Nakamura Y et al. · JAMA oncology · (2026) · View on PubMed ↗

Identification of RRM2 as a key regulator of malignant epithelial cells in gastric cancer through single‑cell transcriptomics.

This study used single-cell transcriptomics to identify RRM2 (ribonucleotide reductase regulatory subunit M2) as a regulator of malignant epithelial cell populations in gastric cancer (GC). By analyzing GC and adjacent normal tissues with inferCNV, pseudotime trajectory analysis, and weighted gene co-expression network analysis, the authors identified RRM2 as a core gene associated with malignant epithelial states and regulatory programs. These results suggest RRM2 could be a potential therapeutic target or biomarker for GC subpopulations defined at single-cell resolution.

Cai X, He Y, Kang L et al. · Oncology reports · (2026) · View on PubMed ↗ · Free PDF ↗

The Target ALS Global Natural History Study: Cross-platform proteomics to accelerate biofluid biomarker and drug target discovery in amyotrophic lateral sclerosis.

This study used 35-plex isobaric tandem mass tag (TMTpro) proteomics to profile cerebrospinal fluid (CSF) and plasma from control participants and sporadic ALS (sALS) participants in the Target ALS Global Natural History Study (TALS GNHS). It identified 2,875 proteins in CSF and 1,118 proteins in plasma and reported known and novel differentially expressed proteins between controls and sALS. These cross-platform CSF/plasma biomarker and drug-target discovery findings could accelerate development of ALS diagnostics and therapeutics.

Yasui D, Weatherill D, Dugom L et al. · medRxiv : the preprint server for health sciences · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Microenvironment & Tumor–Host Interactions

Stress-adapted cancer-associated fibroblasts as mediators of immunosuppression and therapy resistance.

This review studied how stress-adapted states of cancer-associated fibroblasts (CAFs) mediate immunosuppression and therapy resistance across solid tumors, emphasizing dynamic reprogramming rather than fixed CAF lineages. It highlights that hypoxia, oxidative stress, nutrient deprivation, metabolic pressure, and therapy-induced injury drive transcriptional/metabolic/secretory changes that reinforce tumor-promoting signals, extracellular matrix remodeling, and immune evasion. Scientifically, it frames stress-adaptive CAF programs as actionable targets to improve immunotherapy and other anticancer treatments.

Hu Y, Ge J, Xin M et al. · Cancer letters · (2026) · View on PubMed ↗ · Free PDF ↗

Single-cell transcriptomic analysis reveals tumor-immune determinants of lymph node colonization and progression in thyroid cancer.

This study used single-cell RNA sequencing of tumor-infiltrating leukocytes from primary thyroid tumors and matched metastatic lymph nodes, validated by multiplex immunohistochemistry, to define determinants of lymph node colonization and progression in thyroid cancer. Upon lymph node colonization, thyrocytes and tumor-associated macrophages down-regulated inflammatory cytokine receptor expression, including TNFRSF12A and CX3CR1, reshaping the tumor-immune microenvironment. These findings identify specific immune-receptor programs that may be targeted to prevent or treat nodal metastasis in thyroid carcinoma.

Nguyen AT, Viramontes J, Vazquez I et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Genetics/Epigenetics & DNA Damage/Splicing

Lysine pyruvylation couples glycolytic flux to epigenetic regulation.

The study characterized lysine pyruvylation (Kpy) as a metabolite-driven post-translational modification and investigated its enzymology, substrate landscape, and functional roles. Using biochemical and proteomic approaches, the authors systematically mapped Kpy and linked it to glycolytic flux–coupled regulation of protein function, extending beyond prior STAT1 pyruvylation at lysine 201 and suppression of type I interferon signaling. This establishes Kpy as a new mechanistic bridge between cellular metabolism and epigenetic/protein regulation, with implications for cancer and innate immune control.

Song X, Peng P, Zheng H et al. · Nature metabolism · (2026) · 1 citations · View on PubMed ↗

Structural basis of the regulation by CDK11 kinase of early spliceosome activation and evidence for its proofreading by DHX15 helicase.

This work determined the structural basis of how CDK11 regulates early spliceosome activation and assessed proofreading by the DHX15 helicase. Using cryo-EM, the authors solved a spliceosome stalled by the CDK11 inhibitor OTS964 in an early-activated state (pre-Bact-OTS) shortly after U4 snRNP dissociation, revealing how CDK11 phosphorylation of SF3B1 coordinates U2/U6 core activation. The structural evidence supports a model in which DHX15 helicase contributes to proofreading of early spliceosome assembly, informing mechanisms of splicing fidelity and regulation.

Zhang Z, Kumar V, Panta S et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Ectomesenchyme contributes to epidermal stem cell formation through mesenchymal-to-epithelial transition.

The study examined how ectomesenchyme contributes to epidermal stem cell formation by using lineage tracing, single-cell transcriptome and epigenome analyses, and live imaging in mouse skin development. It found that the interfollicular epidermis largely consists of mesenchymal-lineage cells and that mesenchymal-lineage epidermal progenitors arise from ectomesenchyme via mesenchymal-to-epithelial transition. This identifies a developmental origin for epidermal progenitors and clarifies how mesenchymal programs can generate stem cell–like epidermal populations.

Miura A, Kobayashi Y, Hirose Y et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

G-quadruplex homeostasis is a determinant of PARP inhibitor toxicity in BRCA2-deficient cells.

The study examined how G-quadruplex (G4) DNA homeostasis influences PARP inhibitor toxicity in BRCA2-deficient cells by measuring genome instability and drug sensitivity while manipulating G4 structure levels. Elevated G4 DNA structures were identified as a determinant of genome instability and PARP inhibitor toxicity, whereas suppressing G4 structures conferred PARP inhibitor resistance. This links a specific DNA structural feature to HR-dependent vulnerability and suggests that targeting G4 dynamics could modulate PARP inhibitor response in BRCA2-defective tumors.

Sharma AB, Krwawicz J, Tappenden L et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Molecular architecture of heterochromatin at the nuclear periphery of primary human cells.

This study examined the in situ molecular architecture of heterochromatin at the nuclear periphery in primary human cells using cryo-electron tomography with template matching, subtomogram averaging, and molecular simulations. The authors confidently assigned individual nucleosomes and resolved their in-cell structure to secondary-structure resolution, then predicted linker DNA paths to infer oligo-nucleosome arrangements and higher-order chromatin organization. This provides a high-resolution structural framework for how nuclear-peripheral heterochromatin is organized in human cells, informing mechanistic models of genome regulation.

Kreysing JP, Cruz-León S, Betz J et al. · Nature communications · (2026) · 17 citations · View on PubMed ↗ · Free PDF ↗

Diagnosis and Staging of Patients with Prostate Cancer: Report from the 2025 Advanced Prostate Cancer Consensus Conference (APCCC) Diagnostics.

This article reported the consensus-voting results from the 2025 Advanced Prostate Cancer Consensus Conference (APCCC) Diagnostics, which developed 88 multiple-choice questions across diagnostic topics for prostate cancer management. The key output was the structured set of voted recommendations/questions intended to standardize diagnostic decision-making in advanced prostate cancer (details truncated in abstract). Clinically, this consensus work is designed to guide evidence-based diagnostic pathways and reduce variability in practice.

Fanti S, Turco F, Tombal B et al. · European urology · (2026) · View on PubMed ↗ · Free PDF ↗

Thyroid cancer-associated EZH1 Q571R mutation drives chromatin compaction and H3K27me3 invasion into active chromatin.

This mechanistic cancer study investigated the thyroid cancer-associated EZH1 Q571R mutation using biochemical assays, single-molecule analyses, epigenomic profiling, and transcriptomics to define how it alters PRC2 function. EZH1Q571R increased chromatin compaction and stimulated PRC2-EZH1 catalytic activity, rewiring PRC2–chromatin interactions and enabling PRC2 activity to invade H3K36me2-marked active chromatin. The significance is that this mutation-driven epigenetic reprogramming provides a specific molecular explanation for thyroid tumor biology and suggests EZH1/PRC2 pathways as potential therapeutic targets.

Kim H, Kim DG, Ha S et al. · Molecular cell · (2026) · View on PubMed ↗ · Free PDF ↗

Cyclin K condensates bridge CDK12 to phosphorylate and drive oncogenic YAP activation in hepatocellular carcinoma.

This study examined the role of Cyclin K and the CDK12/CDK13 complex in hepatocellular carcinoma (HCC), focusing on how transcriptional condensates regulate oncogenic YAP activation. Cyclin K formed a regulatory condensate that bridged CDK12-mediated phosphorylation of YAP, with phosphorylation at YAP threonine-398 impairing YAP inhibition and thereby driving YAP activation. The work identifies Cyclin K as an essential vulnerability and mechanistic target to disrupt YAP-driven oncogenic transcription in HCC.

Sun Y, Zhang Y, Yan W et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Yap mediates hippo signaling to balance proliferation and differentiation in the developing glandular stomach epithelium.

This study used mouse genetics plus single-cell RNA sequencing and histology to determine how Hippo signaling and the transcriptional coactivator Yap regulate proliferation versus differentiation in the developing glandular stomach epithelium. Yap deletion reduced epithelial growth, while overexpression of constitutively active Yap expanded the epithelium, and scRNA-seq supported that Yap promotes epithelial proliferation. These results establish Yap as a central Hippo pathway effector controlling stomach epithelial development, informing how organ-specific growth programs are balanced.

Mu R, Liu J, Luo D et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Metabolism & Nutrient/Lipid Signaling

Gut microbiota-derived extracellular vesicles: bridging microbial-host crosstalk in metabolic disorders.

This review article synthesizes current knowledge on gut microbiota-derived extracellular vesicles (including bacterial extracellular vesicles, BEVs) as mediators of microbe–host communication in metabolic disorders. It describes how BEVs are generated and how they deliver bioactive cargo (proteins, lipids, and nucleic acids) to host cells to regulate metabolic and immune homeostasis. Scientifically, it frames BEVs as potential mechanistic links and therapeutic targets for metabolic disease progression.

Ma K, Zhang Q, Jin Z et al. · Cell communication and signaling : CCS · (2026) · View on PubMed ↗ · Free PDF ↗

Lipid metabolism of hepatocyte-like cells supports intestinal tumor growth in Drosophila.

The study investigated how lipid metabolism in Drosophila hepatocyte-like oenocytes supports intestinal tumor growth by mapping a tumor-to-tissue signaling axis involving Pvf1 and TORC1–Hnf4. In adult flies, gut tumors secreted Pvf1 to activate the TORC1-Hnf4 pathway, driving production of very long-chain fatty acids and wax esters required for tumor-associated tracheal growth, and blocking Hnf4 or the elongase mElo suppressed tracheogenesis, tumor progression, and cachexia-like wasting. These results reveal a systemic metabolic dependency of tumors on distant tissue lipid programs and highlight pathway nodes (Hnf4, mElo) as potential intervention points.

Huang K, Miao T, Chen Y et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Dysregulated sphingolipid metabolismdrives pancreatic carcinogenesis through plasma membrane Kras enrichment.

This study investigated how dysregulated sphingolipid metabolism drives pancreatic carcinogenesis by focusing on acid sphingomyelinase (SMPD1)–mediated conversion of sphingomyelin (SM) to ceramide (CER) and its relationship to plasma membrane KRAS enrichment. Using targeted quantitative plasma metabolomics in patients with pancreatic cancer (population details truncated in abstract), the authors linked SMPD1-driven sphingolipid shifts to mechanisms that promote KRAS localization and tumor-promoting signaling. These results suggest that SMPD1/sphingolipid pathways and plasma lipid profiles could serve as mechanistic targets and potential biomarkers in pancreatic cancer.

Alnatsha A, Xu J, Habshi T et al. · Gut · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting cholesterol esterification sensitizes liver cancer to CD8+ T cell attack by impairing metabolic and redox resilience.

This study integrated proteomic profiling of human hepatocellular carcinoma (HCC) samples from liver transplant patients with recurrence status and CD8+ T cell killing assays to identify mechanisms of immune evasion, focusing on the cholesterol esterification enzyme SOAT1 (also known as ACAT1). Genetic or pharmacologic inhibition of SOAT1 sensitized liver cancer cells to CD8+ T cell–mediated immunosurveillance and enhanced responses to anti–PD-1 therapy and CAR-T cell therapy, with increased intratumoral CD8+ T cell infiltration. The scientific and clinical significance is that targeting cholesterol esterification via SOAT1 may be a tractable metabolic strategy to improve immunotherapy effectiveness in HCC.

Gu Y, Zhang L, Li J et al. · Immunity · (2026) · View on PubMed ↗

Drosophila storage proteins promote both the rate and the duration of tumor growth.

This study used Drosophila cachectic and noncachectic tumor models to test how fat body-derived storage proteins (hexamerins) contribute to tumor growth, including selective uptake into tumors. Hexamerin uptake supported both the rate and duration of tumor growth by providing nutrients and by promoting tumor expression of the relaxin-like insulin-like protein Dilp8, which inhibited ecdysone production to extend the growth period. These findings link tumor nutrient scavenging to endocrine control of growth timing, suggesting conserved metabolic–hormonal vulnerabilities for cancer progression.

Valzania L, Blanco-Obregon D, Alami A et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

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Cardiovascular Critical Care & Hemodynamics

Post-thrombectomy angiography-derived fractional flow is associated with functional outcomes in ICAS-related large vessel occlusion.

This retrospective analysis of a prospectively maintained registry studied whether post-thrombectomy angiography-derived fractional flow (FF) predicts 90-day functional independence in anterior circulation intracranial atherosclerotic stenosis (ICAS)-related large vessel occlusion (LVO). The key finding was that post-thrombectomy FF was associated with functional outcomes and performed better than purely anatomic stenosis measures (calculation method truncated in abstract). Clinically, FF could help refine post-thrombectomy risk assessment and guide management of residual stenosis in ICAS-LVO.

Yang YN, Yi T, Miao J et al. · Journal of neurointerventional surgery · (2026) · View on PubMed ↗ · Free PDF ↗

Discontinuation of Oral Anticoagulation After Successful Catheter Ablation for Atrial Fibrillation: Meta-analysis of Randomized Clinical Trials.

This meta-analysis of randomized clinical trials studied whether discontinuing oral anticoagulation (OAC) after successful catheter ablation (CA) for atrial fibrillation (AF) is as effective and safe as continuing OAC in AF patients with stroke risk factors. The pooled RCT evidence compared post-ablation OAC discontinuation versus continuation for outcomes including thromboembolism/stroke and bleeding risk. If supported by the trial data, this could inform guideline refinement toward individualized anticoagulation duration after successful CA.

Kaisaier W, Chen Y, Dong Y et al. · Thrombosis and haemostasis · (2026) · View on PubMed ↗

Timing of veno-arterial extracorporeal membrane oxygenation in cardiogenic shock: A systematic review and meta-analysis.

This systematic review and meta-analysis evaluated whether early initiation versus delayed initiation of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) improves outcomes in patients with cardiogenic shock. The analysis compared studies with explicit timing definitions and synthesized evidence registered in PROSPERO (CRD42025635381). Determining the optimal VA-ECMO timing is clinically significant because it may guide critical-care protocols to improve survival and recovery in cardiogenic shock.

Yuan XK, Shi R, Zhang LM et al. · Journal of intensive medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Cardiovascular Risk, Prevention & Epidemiology

PCSK5 promotes angiogenesis and cardiac repair after myocardial infarction.

This study examined the role of the proprotein convertase PCSK5 in myocardial infarction (MI) by analyzing patient plasma and cardiac endothelial cells and testing endothelial-specific genetic manipulation in mouse models. PCSK5 levels were elevated in MI patients, endothelial Pcsk5 deficiency impaired angiogenesis and cardiac repair, and endothelial-specific Pcsk5 delivery enhanced post-MI angiogenesis and cardiac function. Mechanistically, PCSK5 directly cleaved VEGFA to activate angiogenic signaling, suggesting PCSK5 as a therapeutic target to improve cardiac recovery after ischemic injury.

Guo J, Ma S, Ma J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Depth of neutrophil mobilization stratifies survival in ST-elevation myocardial infarction.

The study profiled neutrophil maturation stages in patients with ST-elevation myocardial infarction (STEMI), heart failure, and stroke to determine how depth of neutrophil mobilization stratifies survival. STEMI patients showed the most pronounced engagement of immature neutrophil mobilization, including CD16lowCD10neg preneutrophils (preNeus) and a final mitotic neutrophil progenitor, which was associated with disease outcome. This suggests that specific neutrophil maturation signatures could serve as prognostic biomarkers and reflect severity of systemic inflammation in acute cardiovascular disease.

Richter M, von Göwels J, Fähndrich M et al. · Nature cardiovascular research · (2026) · View on PubMed ↗ · Free PDF ↗

Delayed molecular aging, preservation of energy metabolism and enhanced exercise response in exercise-trained human muscle.

The study analyzed how exercise training alters age-related molecular changes in human skeletal muscle by performing transcriptomics, lipidomics, and metabolomics in young and older adults with different fitness levels before and after an acute submaximal exercise bout. At baseline, older adults showed reduced expression of genes for cellular respiration and energy metabolism, and trained older adults lacked about half of these age-related differences, producing profiles closer to those of fitter individuals. These results indicate that exercise training preserves energy-metabolism programs and shapes the molecular response to exercise, informing interventions to promote healthy aging.

Janssens GE, Trętowicz MM, Grevendonk L et al. · Nature aging · (2026) · View on PubMed ↗ · Free PDF ↗

Long-term trajectories of basal metabolic rate and risk of depressive symptoms: evidence from three large population-based cohorts.

This study analyzed long-term trajectories of basal metabolic rate (BMR) and their association with later depressive symptoms in middle-aged and older adults using three population-based cohorts (CHARLS, HRS, and SHARE). Group-based trajectory modeling identified distinct BMR patterns over time, and logistic regression tested how these trajectories related to incident depressive symptoms. The findings clarify whether changes in metabolic rate across adulthood predict depression risk, informing potential metabolic or lifestyle prevention strategies.

Fu X, Gao X, Kong L et al. · Journal of affective disorders · (2026) · View on PubMed ↗

Suicide mortality in Brazil: Post-pandemic excess mortality and spatial inequalities.

This ecological time-series study examined suicide mortality in Brazil from 2005–2024, assessing post-pandemic excess mortality, spatial inequalities, seasonality, and projections to 2030. Using Brazilian Mortality Information System data and ICD-10 codes X60–X84, it quantified temporal trends and geographic clustering and estimated future burden. The results are significant for public health planning by identifying where and when suicide risk is rising and how it may evolve after the pandemic.

Leão-Cordeiro JAB, Nogueira DJ, Silva AMTC · Journal of affective disorders · (2026) · View on PubMed ↗ · Free PDF ↗

Prevention of Heart Failure in Women: An Expert Consensus Statement on Sex-Specific Risk Factors.

This expert consensus statement reviewed sex-specific risk factors and life-course conditions affecting heart failure (HF) prevention and management in women. The key message was that conventional HF risk prediction often omits sex-specific hormonal and pathology drivers, and prevention strategies should be tailored across specific female conditions (including pregnancy-related hypertensive disorders, among others). Clinically, it provides a roadmap to improve HF outcomes in women by integrating sex-specific risk assessment and management.

Rakisheva A, Disabato G, Abreu A et al. · European journal of heart failure · (2026) · View on PubMed ↗

EAT-Lancet Diet, Plasma Metabolites, and Risk of Peripheral Artery Disease: A Prospective Cohort Study.

This prospective cohort study in 192,166 UK Biobank participants tested whether the EAT-Lancet diet index predicts peripheral artery disease (PAD) risk and used a metabolomics approach to probe mechanisms. Using elastic net regression to derive a diet-related plasma metabolic signature in a subcohort (n=93,961), it evaluated associations between the metabolic signature and PAD risk via Cox proportional hazards models. The study links a sustainable dietary pattern to PAD risk and identifies candidate metabolic pathways that may mediate diet–vascular disease relationships.

Zhang Z, Ren J, Sun X et al. · Journal of the American Heart Association · (2026) · View on PubMed ↗ · Free PDF ↗

Longitudinal Associations of Cumulative Depression Burden With Cardiovascular Diseases and All-Cause Death Among Middle-Aged and Older Population: Evidence From 2 Nationwide Cohort Studies.

This study examined how cumulative depression symptom burden relates to cardiovascular disease (CVD) risk and all-cause mortality among adults aged ≥50 years in two national cohorts from China (CHARLS) and Mexico (MHAS). Using Cox proportional hazards models and quantifying cumulative burden via the area under the curve of repeated depression scores and the number of depression waves, higher cumulative depression burden was associated with increased risks of CVD and death. These findings support the clinical importance of long-term depression monitoring and sustained mental-health intervention as part of cardiovascular risk reduction in older populations.

Tu Q, Liu R, Zheng J et al. · Journal of the American Heart Association · (2026) · View on PubMed ↗ · Free PDF ↗

LDL-cholesterol distance to target: A practical tool for guiding lipid-lowering treatment decisions.

This article proposed and discusses the clinical concept of “LDL-cholesterol distance to target” as a practical tool to guide lipid-lowering treatment decisions beyond simply achieving guideline LDL-C targets. It frames cumulative LDL-C exposure over time as a key determinant of atherosclerotic cardiovascular disease (ASCVD) risk and argues for more proactive, personalized, and sustained early intensive lipid lowering aligned with updated ESC/EAS dyslipidemia guidance. The approach aims to improve treatment selection and monitoring by quantifying how far a patient remains from individualized LDL-C goals.

Palloni MC, Farella T, Faggiano A et al. · Atherosclerosis plus · (2026) · View on PubMed ↗ · Free PDF ↗

Associations of Dietary Patterns and Micronutrients With Major Adverse Cardiovascular Events and Mortality Among Populations With Cardiovascular-Kidney-Metabolic Syndrome Stages 0-3: Results From Two Prospective Cohorts.

This cohort analysis assessed whether dietary patterns and micronutrient intake are associated with major adverse cardiovascular events (MACE) and mortality among people with cardiovascular-kidney-metabolic (CKM) syndrome stages 0–3 using NHANES 2005–2018 and UK Biobank data. It calculated plant-based diet and inflammatory diet scores (including dietary inflammatory index and alternative Mediterranean diet in NHANES; AMED and healthful plant-based diet index in UKB) and tested associations with outcomes using multivariable models. The study’s findings (as reported in the truncated abstract) are intended to clarify which diet-quality and micronutrient patterns may reduce or increase cardiovascular risk in CKM-spectrum populations.

Hou Y, Yuan K, Xu Y et al. · Food science & nutrition · (2026) · View on PubMed ↗ · Free PDF ↗

Frailty as a predictor of adverse in-hospital outcomes in older patients with Takotsubo cardiomyopathy.

This retrospective study evaluated whether frailty predicts adverse in-hospital outcomes in older adults hospitalized with Takotsubo cardiomyopathy (TCM). Using the National Inpatient Sample (2016–2021) and Johns Hopkins ACG frailty-defining diagnoses to classify patients aged ≥65 years, it assessed associations between frailty status and outcomes after multivariable adjustment. Clinically, frailty stratification could help identify higher-risk older TCM patients for targeted management and monitoring.

Bahar AR, Bahar Y, Sirekulam V et al. · Journal of geriatric cardiology : JGC · (2026) · View on PubMed ↗

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Cardiometabolic Disease & Metabolic Therapies (incl. diabetes, MASLD)

Association of C-Reactive Protein-Triglyceride Glucose Index With Chronic Obstructive Pulmonary Disease: Results From the NHANES and CHARLS Cohorts.

This study assessed whether the C-reactive protein–triglyceride glucose index (CTI) is associated with chronic obstructive pulmonary disease (COPD) prevalence in 8682 participants from CHARLS (China) and 8986 participants from NHANES (USA). Using multivariable logistic regression, the authors evaluated the relationship between CTI and COPD and tested the robustness of the association across cohorts (details truncated in the abstract). If CTI reliably tracks COPD risk, it could support a clinically usable biomarker integrating inflammation and insulin resistance.

Gan J, Chen L, Zhu Y · Mediators of inflammation · (2026) · View on PubMed ↗ · Free PDF ↗

A Non-Canonical Role for Hepatocyte MLKL in Promoting Mitochondrial Dysfunction and Senescence in the Aging Liver.

This work investigated hepatocyte-specific functions of the necroptosis effector MLKL in aging liver, focusing on mitochondrial dysfunction and senescence in the setting of metabolic dysfunction-associated steatotic liver disease (MASLD). MLKL in hepatocytes promoted mitochondrial impairment and senescence through necroptosis-independent mechanisms, despite RIPK3 being suppressed in hepatocytes under metabolic disease. The results support targeting MLKL to mitigate inflammatory and metabolic aging phenotypes in the liver beyond canonical necroptosis.

Mohammed S, Jiang C, Pennington T et al. · Aging cell · (2026) · View on PubMed ↗

Glucagon-like peptide-1 receptor agonists versus dipeptidyl peptidase-4 inhibitors after liver resection for hepatocellular carcinoma in patients with type 2 diabetes: a target trial emulation study.

This target trial emulation study compared postoperative incretin-based therapy choices in patients with type 2 diabetes (T2D) undergoing curative-intent liver resection for hepatocellular carcinoma (HCC), using electronic medical records from 36 hospitals in China (2014–2023). It evaluated whether initiating glucagon-like peptide-1 receptor agonists (GLP-1RAs) versus dipeptidyl peptidase-4 inhibitors (DPP-4is) was associated with improved recurrence-free and overall survival (outcome results truncated in abstract). If confirmed, the findings could influence postoperative medication selection to reduce HCC recurrence in T2D patients.

Xiang YJ, Liu ZH, Feng JK et al. · Gut · (2026) · View on PubMed ↗ · Free PDF ↗

Efficacy of tirzepatide versus SGLT2 inhibitors in metabolic dysfunction-associated steatotic liver disease (MASLD): a multicenter propensity-matched real-world study.

This multicenter retrospective propensity score–matched real-world study compared tirzepatide (dual GLP-1/GIP receptor agonist) versus SGLT2 inhibitors in 43,743 new tirzepatide initiators matched 1:1 to 43,743 SGLT2i users with metabolic dysfunction-associated steatotic liver disease (MASLD) and at least one metabolic comorbidity using the TriNetX US Collaborative Network. Tirzepatide was associated with better clinical outcomes than SGLT2 inhibitors (primary outcome details were truncated in the abstract). These findings support tirzepatide as a potentially more effective pharmacologic option for MASLD in routine practice, pending confirmation in prospective trials.

Khalil I, Sarker P, Nur N et al. · Hepatology international · (2026) · View on PubMed ↗

From the Vitamin D Paradox to Precision Nutrition: Targeted Supplementation, Assay Pitfalls, and Clinical Decision-Making.

This narrative review synthesized evidence on vitamin D testing and supplementation, focusing on why observational associations often fail in randomized trials and highlighting assay pitfalls and precision-nutrition decision-making. The key conclusion was that discordance between 25(OH)D observational findings and RCT results is strongly influenced by factors such as assay limitations, baseline vitamin D status, dosing strategies, and targeted testing rather than universal supplementation. Clinically, the review argues for more precise, evidence-based vitamin D management that accounts for measurement quality and patient-specific risk.

Dalamaga M, Tsilingiris D, Petropoulou D et al. · Current nutrition reports · (2026) · View on PubMed ↗ · Free PDF ↗

Ketogenic diet, cardiometabolic diseases and aging.

This narrative review summarized evidence on how the ketogenic diet (KD) affects cardiometabolic diseases and aging. It highlighted roles for ketone bodies such as β-hydroxybutyrate as both energy substrates and signaling molecules influencing vascular, metabolic, and epigenetic pathways, with reported effects on endothelial function, cardiac energy metabolism, lipid profile, and blood pressure. The scientific significance is that KD may represent a modifiable nutritional strategy for cardiometabolic risk and age-related decline, warranting further mechanistic and clinical validation.

Cioffi G, Cuomo G, Carluccio R et al. · Journal of geriatric cardiology : JGC · (2026) · View on PubMed ↗

Metformin modifies hormone changes associated with androgen deprivation therapy for prostate cancer.

This phase III, double-blind randomized controlled trial analysis tested whether metformin modifies laboratory hormone changes associated with androgen deprivation therapy (ADT) in prostate cancer patients. In PRIME (166 normoglycemic patients randomized to metformin vs placebo while receiving ADT), serum samples from 47 metformin and 32 placebo participants were analyzed for biomarkers linked to metabolic syndrome and type II diabetes risk. The significance is that metformin may mitigate ADT-associated metabolic and hormonal toxicity, informing strategies to reduce long-term cardiometabolic complications in prostate cancer care.

Gorman M, Usmani N, Pollak MN et al. · Endocrine oncology (Bristol, England) · (2026) · View on PubMed ↗ · Free PDF ↗

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Renal/Inflammation in Critical Illness (CRRT membranes, AKI)

Clinical applications of oXiris membranes: Targeting inflammation and renal dysfunction in ICU patients.

This article reviewed clinical applications of oXiris membranes, a modified poly(ethersulfone)/AN69 continuous renal replacement therapy membrane designed to adsorb inflammatory mediators and endotoxins, in ICU patients. It reported use across conditions including sepsis/septic shock, intra-abdominal infection, acute kidney injury, and cardiogenic shock (including during VA-ECMO), with emphasis on immunomodulation alongside renal support. The clinical significance is that oXiris may help target inflammation-driven organ dysfunction in critically ill patients, potentially improving outcomes in immune dysregulation states.

Cutuli SL, Lassola S, Philippe R et al. · Journal of intensive medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Infectious Disease & Transmission Blocking

PfApiAT2 is a proline transporter essential for the transmission of Plasmodium falciparum by the mosquito vector.

The study investigated the proline transporter PfApiAT2 in Plasmodium falciparum and its role during mosquito-stage development in Anopheles gambiae. PfApiAT2 was shown to be proline-specific and essential for early oocyst development, with pfapiat2 mutants producing stunted oocysts and severely reduced sporozoite formation, phenotypes that were linked to halofuginone resistance. This identifies PfApiAT2 as a potential transmission-blocking target for malaria control by disrupting parasite development in the mosquito vector.

Khushu M, Kissel RC, Kauffman J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Reproductive Health, Fertility & Pregnancy

Pathophysiology-Based Classification of Male Infertility: Evidence from an 800-patient Prospective Cohort.

This prospective monocentric cohort study (800 male partners of infertile couples) aimed to phenotypically define male factor infertility (MFI) and create a pathophysiology-based classification beyond semen-analysis-only “idiopathic” labeling. By integrating comprehensive evaluation results, the study developed a framework to reduce idiopathic infertility and better align patients with underlying endocrine/pathophysiological mechanisms (specific category outcomes are truncated in the abstract). A mechanistic classification could enable more targeted management strategies for men with infertility.

Grande G, Graziani A, Caretta N et al. · The Journal of clinical endocrinology and metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

Oral microbiome modulation mitigates hyperglycemia exacerbation in gestational diabetes mellitus.

This study investigated oral microbiome dynamics in 534 pregnant women with gestational diabetes mellitus (GDM) and in mouse/cellular models to test whether dysbiotic oral communities worsen hyperglycemia and periodontal inflammation. GDM was associated with a progressive shift from Streptococcus-dominated oral microbiota to Prevotella/Porphyromonas-enriched dysbiosis that induced periodontal inflammation and systemic IL-17/IL-1β responses, exacerbating glucagon-like peptide-1 (GLP-1)–related dysregulation (truncated in abstract). These findings suggest that oral microbiome modulation could be a clinically actionable strategy to mitigate metabolic deterioration and inflammatory pathways in GDM.

Gao S, Yin N, Wei R et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

EGR1 Mediates Ursodeoxycholic Acid-Promoted Mitophagy to Prevent Postovulatory Aging of Porcine Oocytes.

This Aging Cell study investigated the upstream transcriptional regulator Early Growth Response 1 (EGR1) in porcine postovulatory oocyte aging (POA) and tested whether ursodeoxycholic acid (UDCA) can prevent POA via mitophagy. It found that EGR1 downregulation is a key event driving porcine oocyte aging and that UDCA upregulated EGR1, promoting EGR1-mediated mitophagy to prevent POA. These results identify EGR1 as a mechanistic target and suggest UDCA as a potential intervention to improve fertility outcomes and assisted reproductive technology success.

Zhang Y, Han Q, Liu Y et al. · Aging cell · (2026) · View on PubMed ↗ · Free PDF ↗

Risk of Major Malformations Following First-Trimester Exposure to Cariprazine: Preliminary Data From the MGH National Pregnancy Registry for Psychiatric Medications.

This preliminary analysis from the MGH National Pregnancy Registry for Psychiatric Medications assessed major malformation risk after first-trimester exposure to cariprazine in infants of mothers with psychiatric illness, compared with unexposed controls. The key finding was the registry’s early estimate of major malformation risk following cariprazine exposure (full numerical results were truncated in the abstract). Clinically, it provides ongoing pharmacovigilance evidence to inform risk counseling for pregnant patients who may require cariprazine.

Viguera AC, Freeman MP, Slaby EK et al. · Bipolar disorders · (2026) · View on PubMed ↗

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Musculoskeletal/Neuromuscular Pain & Rehabilitation

Comparative Effectiveness of AI-Assisted Telerehabilitation, Telerehabilitation, In-Person Care, and Usual Care for Chronic Nonspecific Low Back Pain: Bayesian Network Meta-Analysis.

This Bayesian network meta-analysis compared AI-assisted telerehabilitation (TLRH-AI), telerehabilitation without AI, in-person rehabilitation (IPR), and usual care (UC) for chronic nonspecific low back pain in patients undergoing rehabilitation. The analysis synthesized comparative effects on pain, disability, kinesiophobia, and health-related quality of life across modalities. The results are intended to guide selection of the most effective remote or in-person rehabilitation strategy, including whether adding AI improves outcomes.

Gu P, Yan Y, Tang H et al. · Journal of medical Internet research · (2026) · View on PubMed ↗ · Free PDF ↗

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Immunology & Inflammatory Signaling (non-cancer; incl. RA, complement, skin JAK-STAT)

Mechanosensing by T cells promotes a tissue-resident memory transcriptional program.

The study examined how activated human T cells sense tissue mechanical stiffness and how this mechanosensing alters nuclear envelope composition, DNA repair initiation, and transcriptional programs in the context of tissue-resident memory. Increased mechanical input drove force-protective DNA repair and reprogrammed expression of core tissue-resident memory genes across diverse tissues. These findings identify mechanotransduction as a regulator of tissue-resident memory formation and suggest that mechanical cues may be leveraged to improve immunotherapies and tissue immunity.

Postat J, Merino M, Mingarelli AR et al. · Nature immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Atypical signaling, ligand recognition and selective agonist discovery of complement receptor C5aR2.

The study investigated biased signaling and ligand recognition of complement receptor C5aR2 by determining cryo-electron microscopy structures of β-arrestin 1–bound C5aR2 and C5aR1 in response to C5a or the metabolite C5a desArg, alongside functional assays. Structural determinants were found that prevent G protein coupling and confer intrinsic bias toward β-arrestin signaling for C5aR2. This provides a molecular framework for selective agonist discovery and for understanding C5aR2-driven immunomodulation in complement-mediated pathology.

Qin J, Cai C, Shan M et al. · Cell research · (2026) · View on PubMed ↗

Genetic biomarkers of clinical manifestations in giant cell arteritis define distinct patient subgroups.

This genome-wide association study analyzed genetic risk factors in 3498 patients with giant cell arteritis (GCA) and 15,550 controls to identify genetic biomarkers linked to specific clinical manifestations. The study found that genetic architecture differs across GCA manifestations, enabling definition of distinct patient subgroups based on genetic biomarkers (functional annotation and specific genes truncated in abstract). This could improve precision phenotyping and risk stratification for GCA, potentially informing tailored diagnostic and therapeutic approaches.

Borrego-Yaniz G, Fuentes-Moreno V, Ortiz-Fernández L et al. · Annals of the rheumatic diseases · (2026) · View on PubMed ↗

PD-1 signalling restrains pathogenic T peripheral helper and effector CD4⁺ T cell functions in rheumatoid arthritis.

This study investigated how inhibitory receptor signaling—especially PD-1—regulates pathogenic T peripheral helper and effector CD4+ T cell functions in rheumatoid arthritis (RA) using CD4+ T cells from RA synovial fluid and control tonsils/blood. In coculture systems with artificial antigen-presenting cells expressing PD-L2 (and other ligands), PD-1 signaling restrained pathogenic CD4+ T cell effector programs and modulated T–B cell interactions (details truncated in abstract). These results support PD-1 pathway agonism as a potential therapeutic strategy to dampen pathogenic T cell activity in RA.

Higashioka K, Sowerby JM, Marks KE et al. · Annals of the rheumatic diseases · (2026) · View on PubMed ↗ · Free PDF ↗

Comparative Efficacy of Biologic Agents for Severe Chronic Rhinosinusitis with Nasal Polyps: A Systematic Review and Network Meta-analysis.

This systematic review and network meta-analysis compared seven biologic agents—dupilumab, omalizumab, mepolizumab, benralizumab, depemokimab, tezepelumab, and stapokibart—for severe chronic rhinosinusitis with nasal polyps (CRSwNP) using randomized trial evidence. It assessed comparative efficacy and safety based on changes in nasal-polyp score (NPS) and nasal congestion score (NCS) at 20–24 and 48–56 weeks, along with smell and patient-reported outcomes. Clinically, the network ranking can help clinicians choose the most effective biologic for severe CRSwNP based on expected symptom improvements and tolerability.

Ouranos K, Michael M, Mylona EK et al. · The Journal of allergy and clinical immunology · (2026) · View on PubMed ↗

Nipocalimab and other FcRn blockers in neuromuscular disorders.

This article reviewed Fc receptor neonatal (FcRn) blockade in autoimmune neuromuscular disorders, focusing on nipocalimab as a fully human high-affinity IgG1 monoclonal antibody. By blocking FcRn–IgG interactions, nipocalimab accelerates pathogenic IgG degradation while sparing other immunoglobulin classes and cellular immune responses. This mechanism suggests a targeted alternative to broader immunosuppression (e.g., IVIG, plasma exchange, steroids) with potential for faster onset in IgG-mediated neuromuscular diseases.

Khateb M, Bril V · Pharmacology & therapeutics · (2026) · View on PubMed ↗

Chronic pain and stress: unravelling the common neuroinflammatory, immune and endocrine mechanisms for novel therapeutic approaches.

This review studied the shared neuroinflammatory, immune, and endocrine mechanisms linking chronic pain and stress to identify novel therapeutic targets. It synthesizes evidence for dysregulation of the sympatho-adrenomedullary system and HPA axis, neuroimmune crosstalk, neurotransmitter and cytokine imbalance, maladaptive neuroplasticity, and peripheral immune activation/autoantibody-mediated sensitization. The mechanistic integration supports development of therapies that interrupt the bidirectional stress–pain cycle rather than treating pain or stress in isolation.

Tékus V, Borbély É, Zelena D et al. · Progress in neuro-psychopharmacology & biological psychiatry · (2026) · View on PubMed ↗

Aryl hydrocarbon receptor deficiency triggers the activation of γδT17 cells to exacerbate autoimmune inflammation.

This mechanistic immunology study investigated how aryl hydrocarbon receptor (AhR) deficiency affects activation of IL-17–producing γδ T cells (γδT17) and thereby exacerbates autoimmune inflammation. AhR was reduced upon γδT17 activation, and AhR deficiency promoted γδT17 activation whereas pharmacologic AhR activation suppressed it, mediated by altered HSPA9 competition with FBXW11 for binding to the RAM domain of Notch intracellular domain (NICD) and impaired FBXW11-dependent NICD ubiquitination. The significance is that AhR–Notch axis regulation of γδT17 activation identifies a potential target for controlling autoimmune inflammatory responses.

He Y, Guo Y, Shi Y et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

JAK-STAT pathway-associated skin diseases: a refined functional framework for inflammatory skin diseases.

This review provided a refined functional framework for inflammatory skin diseases organized around the JAK-STAT signaling pathway. It highlights that small-molecule JAK inhibitors (JAKi) have demonstrated efficacy in conditions such as atopic dermatitis (e.g., abrocitinib, upadacitinib) and psoriasis and alopecia areata/vitiligo (e.g., baricitinib and other approved agents), linking cytokine-driven signaling to disease phenotypes. The article’s significance is to help clinicians and researchers map specific inflammatory skin diseases to actionable JAK-STAT biology and therapeutic targets.

Li B, Song X, Shan C et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Macrophage spatiotemporal plasticity in pulmonary diseases: decoding the niche at single-cell resolution.

This review synthesized evidence on macrophage spatiotemporal plasticity in pulmonary diseases, emphasizing how macrophage states vary by lung niche rather than fitting a simple M1/M2 dichotomy. It integrates findings from single-cell RNA sequencing and spatial multi-omics to describe macrophage functional programs in homeostasis and in chronic obstructive pulmonary disease (COPD). The work is significant because it provides a more precise, niche-aware framework that can guide future biomarker discovery and macrophage-targeted therapies in lung disease.

Lin C, Huang S, Yang L et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

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Clinical Trials, Guidelines & Diagnostic/Imaging Frameworks

Adeno-Associated Virus Gene Therapy for Spinal Muscular Atrophy Induces Hepatotoxicity via Cytokine and Macrophage Activation.

This case-based study investigated mechanisms of hepatotoxicity after adeno-associated virus (AAV) gene therapy in two spinal muscular atrophy patients treated with AAV9 delivering onasemnogene abeparvovec. Shortly after infusion, both patients developed macrophage activation syndrome–like features including marked hyperferritinemia, hepatotoxicity, thrombocytopenia, hypertriglyceridemia, and hypofibrinogenemia, alongside innate immune activation with serial cytokine/chemokine profiling and flow cytometry. The findings implicate cytokine- and macrophage-driven innate immune activation as a mechanistic contributor to AAV9-associated liver injury, informing monitoring and risk mitigation.

Sakai A, Sugiyama M, Onodera M et al. · Liver international : official journal of the International Association for the Study of the Liver · (2026) · View on PubMed ↗ · Free PDF ↗

Myelodysplastic Syndromes: 2026 Update on Diagnosis, Risk-Stratification and Management.

This 2026 update article summarizes current approaches to diagnosis, risk stratification, and management of myelodysplastic syndromes (MDS), a heterogeneous myeloid disorder with cytopenias and risk of progression to acute myeloid leukemia (AML). It emphasizes that diagnosis relies on bone marrow morphology plus complementary testing such as karyotyping, flow cytometry, and molecular genetics under the 2022 WHO framework. Clinically, the review consolidates how modern molecular and cytogenetic data improve prognostication and guide treatment selection in MDS.

Garcia-Manero G · American journal of hematology · (2026) · View on PubMed ↗

Immunonutrition in Early Life: The Role of Complementary Feeding, Dietary Patterns, and Nutritional Exposures on the Health of Young Children-An EAACI Scoping Review.

This EAACI scoping review mapped evidence on how early-life complementary feeding—covering dietary patterns, timing, and nutritional exposures—affects immune development and outcomes such as allergy, infection, growth, and immune endpoints in infants and toddlers (≤3 years). Following PRISMA-ScR and searches through November 2024, the review synthesized evidence across feeding practices (including allergen introduction timing and supplementation/ultra-processed foods) and identified evidence gaps (details truncated in the abstract). The work helps prioritize research directions for immunonutrition strategies during the critical complementary feeding window.

Venter C, Beltran J, Bracchiglione J et al. · Allergy · (2026) · View on PubMed ↗

Predictive factors of response to anti-CGRP pathway drugs in people with multiple sclerosis.

This retrospective multicenter study evaluated predictive factors for response to anti-CGRP pathway drugs in adults with multiple sclerosis (PwMS) who also had migraine, treated with anti-CGRP monoclonal antibodies or gepants alongside stable disease-modifying therapies (DMTs). It compared monthly headache days and analgesic use between treatment initiation and last follow-up to identify factors associated with response (specific predictors and effect sizes are truncated in the abstract). If validated, these predictors could guide personalized migraine treatment choices in PwMS receiving concurrent DMTs.

Nociti V, Cesarano S, Romozzi M et al. · The journal of headache and pain · (2026) · View on PubMed ↗ · Free PDF ↗

Immune aging biomarkers for clinical trials.

This article proposed a translational framework to identify and evaluate immune aging biomarkers for use in clinical trials. It defined five evaluation criteria and applied them to candidate biomarkers, addressing how to quantify immune aging in a trial-ready way. The framework is significant for geroscience-guided interventions because it helps standardize biomarker selection and interpretation when testing therapies aimed at immune rejuvenation.

Cipriano A, Justice J, Poganik JR et al. · Nature medicine · (2026) · View on PubMed ↗

Mitochondrial calcium regulates lipid metabolism by modulating tethering of mitochondria to lipid droplets.

The study examined how mitochondrial calcium regulates lipid metabolism by controlling mitochondria–lipid droplet (LD) tethering in brown adipocytes using an ex vivo reconstitution of mitochondria–LD interactions. Elevated mitochondrial matrix calcium was identified as a potent inducer of mitochondria detachment from LDs, which increases lipolytic activity of recombinant lipases. These findings link mitochondrial Ca2+ signaling to thermogenic lipid catabolism and suggest a mechanistic lever for modulating fat breakdown in metabolic disease.

Acin-Perez R, Assali EA, Veliova M et al. · The EMBO journal · (2026) · View on PubMed ↗ · Free PDF ↗

Semiannual surveillance facilitates detection of surgically treatable intraductal papillary mucinous neoplasm-derived and concomitant carcinoma: a multicenter prospective observational study.

This multicenter prospective observational study evaluated whether semiannual surveillance using endoscopic ultrasonography (EUS) and magnetic resonance imaging (MRI) improves detection of malignant transformation in 360 patients with branch-duct or mixed-type intraductal papillary mucinous neoplasm (IPMN). The key finding was that semiannual surveillance facilitated detection of surgically treatable IPMN-derived and concomitant carcinoma (primary endpoint details truncated in abstract). Scientifically and clinically, it supports a surveillance interval and imaging strategy aimed at catching cancers at a resectable stage.

Ohashi Y, Maruta A, Koizumi T et al. · Pancreatology : official journal of the International Association of Pancreatology (IAP) … [et al.] · (2026) · View on PubMed ↗ · Free PDF ↗

Somatostatin receptor PET response assessment framework for patients with neuroendocrine tumours (V1.0): a modified Delphi consensus from the European Neuroendocrine Tumor Society (endorsed by EANM and NANETS).

This modified Delphi consensus study developed a somatostatin receptor PET response assessment framework for patients with neuroendocrine tumours (NETs) through a structured, multi-round process involving 34 international experts across nuclear medicine, radiology, oncology, endocrinology, and surgery. The key output was a standardized, versioned (V1.0) set of criteria for assessing therapy response using somatostatin receptor PET imaging, reaching consensus on the majority of evaluated statements (≥75%). Standardized somatostatin receptor PET response criteria are clinically significant because they can harmonize trial endpoints and improve comparability of treatment response assessment across NET studies and practice.

Deroose CM, Leupe H, Hicks RJ et al. · The Lancet. Oncology · (2026) · View on PubMed ↗

The Effect of Preoperative Hydration on Cardiac Surgery-Associated Acute Kidney Injury.

This prospective, randomized, controlled single-center trial studied whether preoperative intravenous 0.9% normal saline hydration for 12 hours reduces postoperative renal dysfunction and acute kidney injury in 110 patients undergoing open-heart surgery with baseline renal function preserved. Compared with a control strategy of fluid restriction for 12 hours, the hydration group showed improved postoperative creatinine outcomes and reduced acute kidney injury risk (as reported in the trial results). The significance is that perioperative fluid strategy could be a modifiable factor to prevent cardiac surgery–associated acute kidney injury.

Karakoc AZ, Ozcan E, Akardere OF et al. · Brazilian journal of cardiovascular surgery · (2026) · View on PubMed ↗

Three versus six weeks of corticosteroids for mild immune-related pneumonitis: a randomized trial.

This randomized trial compared a 3-week versus guideline-recommended 6-week corticosteroid taper for patients with mild (CTCAE grade 1–2) immune-related pneumonitis after immune checkpoint inhibitor therapy. The study tested whether the shorter regimen was noninferior in achieving treatment success at 8 weeks, defined by maintaining resting room-air SpO2 ≥90% without steroid escalation or prolongation. The clinical significance is that if noninferiority is confirmed, a shorter steroid course could reduce steroid exposure while maintaining safety and effectiveness for mild ICI-related pneumonitis.

Fujimoto D, Abe M, Murotani K et al. · American journal of respiratory and critical care medicine · (2026) · View on PubMed ↗

Performance of DeepSeek V3.2 and ChatGPT 5.1 in Musculoskeletal Triage and Differential Diagnosis of Outpatients With Low Back Pain: Multidimensional Comparative Study.

This retrospective comparative study evaluated ChatGPT 5.1 and DeepSeek V3.2 for musculoskeletal triage and differential diagnosis of outpatients with low back pain using real-world outpatient records under simulated information conditions. The key finding was that model performance differed by clinical information condition, indicating that diagnostic accuracy and triage effectiveness are sensitive to what information the models receive. Clinically, this supports cautious, condition-aware deployment of large language models for low back pain triage and differential diagnosis workflows.

Ma Z, Chen R, Wang A et al. · Journal of medical Internet research · (2026) · View on PubMed ↗ · Free PDF ↗

Systematic review and meta-analysis of randomized controlled trials: low-intensity extracorporeal shockwave therapy (Li-ESWT) for erectile dysfunction after radical prostatectomy.

This systematic review and meta-analysis synthesized randomized controlled trials (297 participants across five RCTs) to assess low-intensity extracorporeal shockwave therapy (Li-ESWT) for erectile dysfunction after radical prostatectomy. Participants receiving Li-ESWT showed significantly greater improvements in International Index of Erectile Function (IIEF) scores at 8 and 12 weeks compared with controls. These results support Li-ESWT as a potentially effective post–radical prostatectomy intervention for ED, though the evidence quality and trial heterogeneity should be considered.

Zhou Z, Cheng Z, Wei G et al. · International urology and nephrology · (2026) · View on PubMed ↗

N-acetylcysteine for non-paracetamol-induced acute liver failure in children: A systematic review and meta-analysis.

This systematic review and meta-analysis evaluated whether N-acetylcysteine (NAC) improves outcomes in children with non–paracetamol-induced acute liver failure (ALF), searching PubMed and Embase for studies published before 20 August 2025. The analysis focused on overall survival and transplant-free survival as primary outcomes for pediatric NAC-treated non-paracetamol ALF. Scientifically and clinically, it addresses a major evidence gap by testing whether NAC—proven in paracetamol ALF—also benefits pediatric non-paracetamol ALF.

de Groot ADE, Stoppels DM, Bourgonje AR et al. · British journal of clinical pharmacology · (2026) · View on PubMed ↗

The Pterygopalatine Ganglion Within the Pterygopalatine Fossa: Quantitative Topography and Implications for Posteriorly Directed Percutaneous Access.

This Clinical Anatomy study used dissection of 22 pterygopalatine fossae from 11 adult human cadaveric heads to quantify the spatial relationships among the pterygopalatine ganglion (PPG), pterygopalatine fossa walls, and the maxillary artery branches. The key finding was consistent anatomical positioning of the PPG near the posterior wall, enabling identification of safer posteriorly directed percutaneous access pathways. Scientifically and clinically, the morphometric map supports safer planning for radiofrequency, anesthetic blockade, and neuromodulation procedures targeting the PPG.

Barbieri IP, Flores JC, González DL et al. · Clinical anatomy (New York, N.Y.) · (2026) · View on PubMed ↗

A review of the randomized clinical trial results from the Staphylococcus aureus network adaptive platform (SNAP) meticillin-susceptible (MSSA) and penicillin-susceptible (PSSA) domains and CloCeBa.

This review summarized randomized clinical trial results from the Staphylococcus aureus network adaptive platform (SNAP) for meticillin-susceptible S. aureus bloodstream infection/bacteraemia (MSSA) and penicillin-susceptible S. aureus (PSSA) domains, and discussed CloCeBa. The key point was that the SNAP trial highlighted high acute kidney injury rates with high-dose flucloxacillin, challenging long-standing guideline assumptions that flucloxacillin is the default first-line therapy. Scientifically and clinically, it supports re-evaluating antibiotic choice and dosing strategies in MSSA SAB to reduce kidney injury risk.

Goodman AL, Easom N, Bielopolski D et al. · The Journal of antimicrobial chemotherapy · (2026) · View on PubMed ↗ · Free PDF ↗

CGRP-Targeted Therapy in Vestibular Migraine-How Strong Is the Evidence?

This article reviewed evidence for calcitonin gene-related peptide (CGRP)-pathway targeted prevention of vestibular migraine (VM), focusing on monoclonal antibodies (mAbs) and small-molecule receptor antagonists (gepants). Across identified studies (n=8), the authors conclude that available data are limited and potentially biased due to small sample sizes, retrospective designs, lack of blinding, and patient-selection issues, making the strength of evidence for VM-specific efficacy uncertain. The review highlights the need for larger, prospective, blinded trials to define which CGRP-targeted drugs work best for vestibular migraine.

Tarnutzer AA, Castro Abarca P, Kaski D · European journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Duchenne Muscular Dystrophy and Delandistrogene Moxeparvovec Gene Therapy in Children: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis evaluated delandistrogene moxeparvovec gene therapy in children with Duchenne muscular dystrophy (DMD) who are ambulatory. It focused on restoring dystrophin expression via microdystrophin delivery and synthesized evidence on efficacy outcomes across included studies (as described in the truncated abstract). The analysis is clinically important because it helps quantify benefits and informs the evidence base for using this AAV-based gene therapy in pediatric DMD patients.

Antonello BB, Cargnelutti Fontoura F, Braga Albuquerque AL et al. · Neurology. Genetics · (2026) · View on PubMed ↗ · Free PDF ↗

Sexual dysfunction associated with 5α-reductase inhibitors in the treatment of androgenetic alopecia: a systematic review.

This systematic review examined sexual dysfunction adverse events associated with 5α-reductase inhibitors (5-ARIs) used for androgenetic alopecia (AGA). It synthesized evidence that some AGA patients experience decreased libido, erectile dysfunction, and ejaculatory disorders attributable to 5-ARI exposure. Clinically, recognizing this association can improve diagnosis, counseling, and risk–benefit decision-making for men treated with 5-ARIs for hair loss.

Złotowska A, Jastrząb-Miśkiewicz B, Krajewski PK · Frontiers in medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Primary hyperoxaluria type 1-current practice in the siRNA era: an ERA Genes & Kidney Working Group survey.

This cross-sectional international survey assessed current clinical practice for primary hyperoxaluria type 1 (PH1) among clinicians in the siRNA therapeutic era. It evaluated how physicians implement PH1 management and treatment recommendations following recent advances, including siRNA-based options, via an ERA Genes & Kidney Working Group questionnaire. The significance lies in identifying gaps between guideline recommendations and real-world care to improve PH1 treatment implementation and patient outcomes.

Bartram MP, Capasso G, Cornec-Le Gall E et al. · Clinical kidney journal · (2026) · View on PubMed ↗ · Free PDF ↗

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Generated automatically on July 05, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.