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PubMed Trending Research Digest — August 13, 2026

A curated digest of 96 trending PubMed articles, automatically categorised and summarised across 15 research areas.

PubMed Trending Research Digest — August 13, 2026

Automated digest · 96 articles · 15 research areas · August 13, 2026

Overview

Across this week’s set, a dominant theme is precision—either by targeting specific molecular nodes or by stratifying patients with biomarkers and mechanistic signatures. In oncology, multiple studies emphasize how the tumor microenvironment and lineage state shape response (e.g., immunosuppressive stromal features predicting BCG response; CAF–Treg recruitment circuits in lung cancer; fasting-mimicking diets reprogramming tumor immunity). Parallel work in precision oncology highlights actionable dependencies revealed by functional genomics (e.g., aneuploidy-linked chr8 dependencies in MPNST; cortactin–AURKB/ACP1 invasion signaling; resistance mechanisms to KRAS-pathway inhibition in PDAC), while clinical translational efforts expand therapeutic reach (oral PD-L1 inhibition feasibility; HER2-stratified ADoC/ADC evaluation; CAR-T timing strategies).

A second major thread is “mechanism-to-therapy” in non-oncologic disease, especially where stress, inflammation, and immune regulation drive pathology. Several studies connect oxidative/ER stress to NRF2-driven protection or disease initiation (dry AMD vascular injury; PSC), define immune sensing pathways (MDA5 activation by cellular RNA homeostasis disruption; innate immune PRR signaling reviews), and refine immune cell stability (TIF1γ controlling Treg lineage stability). In neurodegeneration and brain aging, work spans from targeted tau dephosphorylation pharmacology to microglial senescence signaling (sDLK1) and large-scale human myeloid state mapping tied to AD risk.

Finally, the digest includes a strong “real-world and implementation” emphasis: guideline updates and comparative evidence (dyslipidemia management; pancreatic RT), registry/observational studies informing safety and effectiveness in routine care (COPD beta-blockers; Atezo/Bev discontinuation drivers; newborn screening impact in SMA), and improved measurement/diagnostic frameworks (pediatric CT dose reference levels; assay performance for myasthenia antibodies; ATI vs AIN adjudication). Together, these papers suggest the field is converging on therapies that are not only more targeted, but also better delivered, monitored, and matched to the right patients.


Critical Care & Sepsis Therapeutics

Ultra-early versus early adjunctive vasopressin initiation after norepinephrine escalation in septic shock: a target trial emulation.

This study emulated a target trial in adults with septic shock from MIMIC-IV (2008–2022) and eICU-CRD (2014–2015) to compare ultra-early adjunctive vasopressin initiation (within 0–3 h) versus early initiation (>3–6 h) after norepinephrine escalation to ≥0.25 μg/kg/min. Ultra-early versus early vasopressin initiation was evaluated using the clone-censor-weight method to estimate cumulative incidence curves, with results reported in the truncated abstract. If ultra-early initiation improves outcomes, it would support earlier vasopressin addition to norepinephrine in septic shock protocols to potentially reduce time-dependent morbidity and mortality.

Nakashima T, Ichinomiya T, Nakajima M et al. · Intensive care medicine · (2026) · View on PubMed ↗


Cancer Immunotherapy & Tumor Microenvironment

A novel CAF population coordinates hyper-suppressive regulatory T cell recruitment and localization in lung cancer.

This study characterized a novel immunomodulatory cancer-associated fibroblast (CAF) population in primary lung adenocarcinoma and pulmonary metastases using single-cell and spatial transcriptomics. The identified imCAFs expressed the cell adhesion molecule CHL1 and were spatially colocalized with CXCR3+ hyper-suppressive regulatory T (Treg) cells at the tumor border, producing CXCL9 to drive CXCR3+ Treg recruitment. These findings define a tumor microenvironment circuit (imCAF–CXCL9–CXCR3+ Treg) that could be targeted to reduce Treg-mediated immune suppression in lung cancer.

Ringham OR, Rivera M, Loffredo LF et al. · Nature immunology · (2026) · View on PubMed ↗

Neoadjuvant Intralesional Daromun (L19IL2/L19TNF) in Resectable Locally Advanced Melanoma: An Update on the Efficacy and Safety Results of the PIVOTAL Phase III Trial.

This phase III PIVOTAL trial update studied neoadjuvant intralesional Daromun (L19IL2/L19TNF) versus up-front surgery in patients with fully resectable stage III melanoma. The key finding was a statistically significant improvement in recurrence-free survival (RFS) with daromun followed by surgery (hazard ratio 0.59; P=.005) at a median follow-up of 21 months. This provides evidence that intralesional IL-2/TNFα–based therapy can improve outcomes in resectable stage III melanoma, potentially changing neoadjuvant treatment strategies.

Hauschild A, Hassel JC, Ziemer M et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

Glofitamab-Based Therapy for Relapsed or Refractory CNS Lymphoma: A Multicenter Retrospective Study.

This multicenter retrospective study evaluated glofitamab-based therapy in 84 patients with relapsed or refractory CNS lymphoma (53 primary CNS lymphoma [PCNSL], 31 secondary CNS lymphoma [SCNSL]). The key finding was high objective response rates (ORR) and complete response rates (CRR) with glofitamab, with outcomes reported separately for monotherapy versus combination therapy in PCNSL and SCNSL. These results support glofitamab as a potential treatment option for R/R CNS lymphoma and help define response expectations in real-world practice.

Xing R, Yang A, Huang J et al. · Blood cancer discovery · (2026) · View on PubMed ↗

Fasting-Mimicking Diets Reprogram Cancer-Associated Fibroblasts to Reverse the Immunosuppressive Tumor Microenvironment in Breast Cancer.

This preclinical study used single-cell transcriptomic sequencing to determine how fasting-mimicking diets (FMD) reprogram the tumor microenvironment in a mouse model of spontaneous breast cancer. The key finding was that FMD suppressed tumor cell stemness, promoted apoptosis, and increased infiltration of innate and adaptive immune cells—especially NK cells and effector CD8+ T cells. These results are significant because they suggest FMD can reverse immunosuppression in breast cancer and may support rational combination strategies with immunotherapies.

Zhang J, Li N, Li R et al. · Cancer research · (2026) · View on PubMed ↗

Nivolumab plus ipilimumab-based treatment in Japanese patients with metastatic non-small cell lung cancer and tumor PD-L1 < 1%: a pooled analysis.

This pooled analysis evaluated first-line nivolumab plus ipilimumab-based regimens in Japanese adults with metastatic non-small cell lung cancer (NSCLC) and tumor PD-L1 <1%, comparing nivolumab+ipilimumab with or without 2 cycles of chemotherapy versus chemotherapy alone using data from CheckMate 227 and CheckMate 9LA. The study focused on long-term, durable outcomes in this high-unmet-need PD-L1–low subgroup. The significance is that it strengthens evidence for immunotherapy benefit in metastatic NSCLC even when PD-L1 expression is <1%, informing treatment selection in Japanese practice.

Nishio M, Hayashi H, Goto Y et al. · International journal of clinical oncology · (2026) · View on PubMed ↗ · Free PDF ↗

The pre-treatment tumor microenvironment immune status determines Bacillus Calmette-Guerin immunotherapy response in early-stage bladder cancer.

This study investigated how the pre-treatment tumor microenvironment immune status predicts response to Bacillus Calmette-Guérin (BCG) immunotherapy in early-stage bladder cancer patients. BCG response was not associated with the number of tumor-infiltrating T cells but was determined by an immunosuppressive pre-treatment microenvironment, including a cancer-associated fibroblast subset characterized by MFAP2+ CAF that impaired BCG-induced antitumor immunity. These findings suggest that baseline immune-suppressive stromal features (e.g., MFAP2+ CAF) could stratify patients likely to respond to BCG and guide combination strategies to overcome resistance.

Guo Y, Ren X, Zhang Z et al. · Cancer immunology research · (2026) · View on PubMed ↗


Cancer Targeted Therapy & Precision Oncology

Mutant p53 reactivation and DNA demethylation in the treatment of AML/MDS.

This translational study evaluated whether arsenic trioxide (ATO) can reactivate mutant p53 and synergize with the DNA hypomethylating agent decitabine in acute myeloid leukemia/myelodysplastic syndromes (AML/MDS) harboring p53 mutations. The key finding is that ATO-rescued mutant p53 strengthens interferon responses by directly transactivating IRF7, and decitabine further enhances ATO-rescued mutant p53 activity via p53 serine-20 phosphorylation while blocking MDM2-mediated inhibition, leading to combined killing of p53-mutant AML cells and suppression of tumor growth (details truncated). Clinically, this supports a rational combination strategy—ATO plus decitabine—to overcome resistance in p53-mutant AML/MDS by coupling p53 reactivation with epigenetic priming of interferon pathways.

Song H, Chen X, Xiao S et al. · Science translational medicine · (2026) · View on PubMed ↗

Acquired resistance to the RAS(ON) multi-selective inhibitor daraxonrasib guides rational combination therapy strategies in pancreatic cancer.

This study analyzed mechanisms of acquired resistance to daraxonrasib, an orally bioavailable RAS(ON) tri-complex inhibitor targeting oncogenic and wild-type N, H, and KRAS, in metastatic pancreatic adenocarcinoma (PDAC). Using targeted sequencing of >800 genes in paired pretreatment and end-of-treatment circulating tumor DNA samples, the authors identified resistance mechanisms that can inform rational combination therapy strategies. These findings are clinically significant for improving durability of RAS(ON) inhibition and guiding next-line combination regimens in RAS-mutant PDAC.

Aronchik I, Kar S, Zhuang Y et al. · Nature medicine · (2026) · View on PubMed ↗

Expanding indications for PARP inhibitors in prostate cancer.

This narrative review studied how to expand clinical indications for poly(ADP-ribose) polymerase inhibitors (PARP inhibitors) in metastatic prostate cancer (mCaP) beyond canonical homologous recombination repair (HRR) gene alterations. It summarizes evidence that PARP inhibitors are effective in patients with HRR alterations such as BRCA1/2 and selected additional DNA damage repair (DDR) genes, and it reviews ongoing combination strategies designed to broaden benefit. The review supports a growing precision-oncology framework for selecting and combining PARP inhibitors to treat a wider fraction of mCaP patients.

Kowalewski HS, Wessels F, Banna GL et al. · Urologic oncology · (2026) · View on PubMed ↗

Trans-regulatory gene mapping prioritizes disease drivers in asthma.

The study introduced DANDELION, a mediation-inspired statistical framework integrating trans-regulatory effects from disease-relevant tissues with gene-level burden from whole-exome sequencing to prioritize disease-proximal genes (DPGs) in asthma. Applying DANDELION to asthma identified novel DPGs that were missed by conventional approaches, and the authors used CRISPR screens in epithelial cells to validate key candidates. This provides a gene-prioritization strategy that can improve identification of causal asthma drivers for downstream functional and therapeutic development.

Salamone IM, Tian P, Qi Z et al. · Cell · (2026) · View on PubMed ↗

Biomarker-Stratified Phase II Trial of Trastuzumab Rezetecan in Advanced Salivary Gland Carcinoma Across Cohorts With High and Low Human Epidermal Growth Factor Receptor 2 Expression.

This phase II, biomarker-stratified trial evaluated trastuzumab rezetecan (SHR-A1811), a HER2-directed antibody-drug conjugate, in advanced salivary gland carcinoma enrolled into prospectively defined HER2-high and HER2-low cohorts. The key finding was that efficacy and safety were assessed separately across HER2 expression strata using immunohistochemistry (IHC) and in situ hybridization (ISH) criteria (HER2-high: IHC 3+ or IHC 2+/ISH+; HER2-low: IHC 1+ or IHC 2+/ISH-). Clinically, the study addresses whether SHR-A1811 can provide benefit in both HER2-high and HER2-low salivary gland cancers where prospective HER2-directed data are limited.

Chen GL, Guo Y, Liu X et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

Acute tubular injury versus acute interstitial nephritis in the kidney precision medicine project.

This Kidney Precision Medicine Project analysis compared acute tubular injury (ATI) versus acute interstitial nephritis (AIN) among the first 60 biopsy-confirmed AKI participants using clinicopathologic adjudication plus pathologic and molecular interrogation. The key finding was that ATI and AIN were frequently misclassified clinically, with 50% adjudicated as ATI and 22% as AIN, highlighting diagnostic uncertainty when biopsies are not obtained. Clinically, the work supports more precise differentiation of ATI vs AIN in AKI, which is crucial because AIN may require different management than ATI.

Schaub JA, Menon R, Melo Ferreira R et al. · JCI insight · (2026) · View on PubMed ↗

Druggable genome CRISPRi screen in hydrogels reveals regulators of cortactin-driven actin remodeling promoting glioblastoma invasion.

The study used druggable genome CRISPRi screens with multiomic profiling in patient-derived glioblastoma cells embedded in biomimetic 3D hydrogels to identify regulators of cortactin-driven actin remodeling that promote invasion. Suppression of 12 druggable genes from 2,550 hits limited invasion, with AURKB (aurora kinase B) and ACP1 (LMW-PTP) validated in neurosphere assays and in vivo, and proximity labeling linking cortactin to LMW-PTP–aurora B signaling. These findings nominate AURKB and ACP1 as actionable targets and define a cortactin phosphorylation axis that could be therapeutically exploited to reduce glioblastoma invasiveness.

Hu M, Weldy A, Lovalvo IM et al. · JCI insight · (2026) · View on PubMed ↗

Combined FAK and MEK inhibition suppresses chromosome 8 gain malignant peripheral nerve sheath tumors.

The study examined how chromosome 8 gain contributes to malignant peripheral nerve sheath tumor (MPNST) pathogenesis, focusing on NF1-associated tumors, and tested combined FAK and MEK inhibition as therapy. Using a CRISPR knockout screen, it identified essential chr8 genes including PTK2 (FAK), and combined inhibition suppressed chr8-gain MPNST growth. This supports a targeted therapeutic strategy that exploits recurrent aneuploidy-associated dependencies in NF1-linked MPNST.

Wang G, Borcherding DC, Wang J et al. · The Journal of clinical investigation · (2026) · View on PubMed ↗

Combined BET bromodomain and DNMT inhibition targets critical survival pathways in transdifferentiated prostate cancer.

The study used multi-omic profiling of TP53/RB1 loss in prostate cancer to identify survival pathways activated during lineage plasticity (including neuroendocrine prostate cancer-like states) and tested combined BET bromodomain and DNMT inhibition. In models of transdifferentiated prostate cancer, dual BET and DNMT inhibition targeted critical survival programs associated with TP53/RB1-driven lineage plasticity and improved therapeutic outcomes. This provides a rationale for epigenetic combination therapy to overcome resistance to androgen receptor (AR) inhibition in aggressive, lineage-plastic prostate cancer.

Storck WK, Flores D, Kumaraswamy A et al. · JCI insight · (2026) · View on PubMed ↗


Cancer Vaccines, Antibodies & Cell Therapies

Viral gene replication enhances AAV vector quality and reduces manufacturing costs.

The study investigated whether using human adenovirus DNA replication machinery in HEK293 cells to amplify plasmid DNA could improve adeno-associated virus (AAV) vector manufacturing. Viral gene replication enabled AAV production with 10–20-fold less plasmid encoding AAV viral genes and achieved up to ~400-fold plasmid amplification to support packaging. This could lower manufacturing costs and reduce plasmid-derived contaminants for AAV gene and cell therapies.

Liu H, Du A, Liu N et al. · Molecular therapy : the journal of the American Society of Gene Therapy · (2026) · View on PubMed ↗

Trials in progress: CARMAN - study protocol of a randomized controlled, international, multicenter, open-label phase II trial evaluating early treatment intensification in patients with high-risk mantle cell lymphoma using CAR-T-cell treatment after an abbreviated induction therapy with rituximab and ibrutinib and 6 months ibrutinib maintenance as compared to standard of care induction and maintenance.

The CARMAN study protocol evaluated a randomized, controlled, international, multicenter phase II strategy for high-risk mantle cell lymphoma (hr MCL) using CAR-T-cell therapy after abbreviated induction with rituximab and ibrutinib plus 6 months of ibrutinib maintenance, compared with standard-of-care induction and maintenance. The trial is designed to test whether incorporating brexucabtagene-autoleucel (brexu-cel; anti-CD19 CAR-T) earlier improves outcomes in hr MCL defined by factors such as high-intermediate/high-risk MIPI-c, p53 overexpression, or TP53 alterations. If successful, this could establish a more effective first-line regimen for hr MCL patients who have poor prognoses with current approaches.

Tilch MK, Schmidt C, Trneny M et al. · BMC cancer · (2026) · View on PubMed ↗

Phase I safety, efficacy, and biomarker response evaluations of three oral PD-L1 inhibitors: INCB086550, INCB099280, and INCB099318.

Three phase 1 open-label, non-randomized dose-escalation/expansion studies evaluated oral small-molecule PD-L1 inhibitors INCB086550, INCB099280, and INCB099318 in patients with advanced solid tumors. The key findings reported were safety, preliminary efficacy, and pharmacokinetic/pharmacodynamic biomarker responses across these agents (with PD-L1 pathway engagement assessed as part of the biomarker program). This supports clinical feasibility of oral PD-L1 inhibition and provides early translational biomarker guidance for further development in solid cancers.

Prenen H, Rottey S, Pinato DJ et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗

Isolation of Novel Fully Human Single-Domain Antibodies Targeting GUCY2C from a Heavy-Chain-Only Transgenic Mouse Platform.

Researchers used a fully human heavy-chain-only transgenic “huNano” mouse platform to isolate novel single-domain antibodies targeting the tumor antigen guanylyl cyclase C (GUCY2C/GC-C). The study generated fully human HcAbs/sdAbs with candidate suitability for downstream GC-C–based CAR-T therapy and bispecific antibody development. This provides a scalable, fully human antibody source against GC-C, supporting therapeutic development for GC-C–expressing cancers.

Zhu P, He L, Du X et al. · Technology in cancer research & treatment · (2026) · View on PubMed ↗

Intratracheal Delivery of mRNA Lipid Nanoparticles Reprograms Alveolar Macrophages for Pulmonary Cancer Immunotherapy.

The study compared intranasal versus intratracheal delivery routes for mRNA lipid nanoparticle (mRNA-LNP) vaccines to determine how route-dependent targeting affects pulmonary cancer immunotherapy in vivo. Intratracheal administration produced a much larger increase in functional mRNA transfection in alveolar macrophages than intranasal delivery, driving stronger tumor-vaccination immunologic effects. These results identify intratracheal delivery as a route that can more effectively program alveolar macrophages for localized lung cancer immunotherapy.

Zhou J, Li T, Zhang W et al. · ACS nano · (2026) · View on PubMed ↗

Repurposing a Small Molecule Plant Hormone as a Tunable ON-Switch for CAR-T Cell Immunotherapy.

This work engineered a plant hormone–based inducible ON-switch CAR-T system using the auxin receptor AFB1 and co-receptor IAA7 to control CAR-T activation in a tunable, ligand-dependent manner. The engineered receptor enabled rapid, reversible, dose-dependent T cell activation with improved control over off-target activity compared with less regulated switch designs. This is scientifically significant because it provides a potentially less immunogenic and more precisely controllable ON-switch strategy for CAR-T immunotherapy safety and efficacy.

Zeng H, Zheng L, Tao R et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗


Cancer Mechanisms & Translational Models

Mechanism of K63-linked polyubiquitin recognition and cleavage by the BRCA1-A complex.

This mechanistic study examined how the BRCA1-A supercomplex (ARISC-RAP80 with BRCA1-BARD1) recognizes and cleaves K63-linked polyubiquitin chains at DNA damage sites. The authors found that a composite three-subunit interface positions K63-linked polyubiquitin into the ARISC-RAP80 catalytic site, with additional RAP80 and ubiquitin-binding sites enforcing a compact substrate conformation that supports recognition and cleavage. Understanding this K63-polyubiquitin processing mechanism is significant for clarifying how BRCA1-mediated DNA damage responses are regulated at the molecular level.

Foglizzo M, Datta A, Degtjarik O et al. · Nature communications · (2026) · View on PubMed ↗

USP8 controls proteostasis pathways in B cells and multiple myeloma.

The study investigated how ubiquitin-specific protease 8 (USP8) regulates proteostasis pathways in B cells and in multiple myeloma (MM), using stage-specific Usp8 deletion in B-cell development in mice and experiments in patient-derived MM cells. USP8 depletion and pharmacologic USP8 inhibition (DUB-IN-2) were used to assess effects on B-cell survival/development and on MM cell sensitivity or resistance to the proteasome inhibitor bortezomib (BTZ). The results support USP8 as a functional vulnerability in MM and a regulator of proteostasis relevant to overcoming or understanding BTZ resistance.

Dufner A, Thery F, Monaco G et al. · Leukemia · (2026) · View on PubMed ↗

Human iPSC-derived heart valve-like assembloids model valve development and disease pathology.

Researchers developed a human induced pluripotent stem cell (iPSC)-derived heart valve-like assembloid platform to model human valve development and disease pathology under controlled mechanical forces and endothelial/shear-stress conditions. They found that sequential mechanical and culture cues promote valve induction, maintenance, and extracellular matrix stratification, and the system recapitulates valve defects driven by genetic mutations, injury, and hyperglycemia-related abnormalities. This provides a human-relevant experimental model to study valve disease mechanisms and test therapeutic strategies targeting human-specific pathology.

He Y, Jalili A, Jones CB et al. · Cell stem cell · (2026) · View on PubMed ↗

Effects of newborn screening and nusinersen on survival and functional outcomes in spinal muscular atrophy with two SMN2 copies: A nationwide multicentre real-world study from Turkey.

Researchers used integrated bulk RNA-seq, single-cell RNA-seq (scRNA-seq), network pharmacology, and experimental validation to identify active constituents and molecular targets of the traditional Chinese medicine Fuzheng Xiaozheng Prescription (FZXZP) against hepatocellular carcinoma (HCC) in a murine model. The study highlighted CCNB1/CDK1-mediated G2/M arrest as a key anti-HCC mechanism associated with FZXZP’s effects on tumor cells. This provides a mechanistic, transcriptomics-driven rationale for FZXZP’s anti-cancer activity centered on cell-cycle blockade.

Komur M, Çağlar E, Akbeyaz İH et al. · European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society · (2026) · View on PubMed ↗

Aberrant O-glycosylation Induces IL-34-Mediated Immune Remodeling and Promotes Pancreatic Cancer Progression.

This mechanistic cancer research study investigated how aberrant O-glycosylation—specifically expression of the Tn antigen (a truncated O-glycan)—drives IL-34–mediated immune remodeling and promotes pancreatic ductal adenocarcinoma (PDAC) progression. The key finding was that Tn expression enhanced PDAC proliferation and tumor growth in vivo and remodeled the tumor immune microenvironment in an IL-34–dependent manner. Scientifically, it identifies a pathway (Tn → IL-34 → immune remodeling) that could be leveraged to improve Tn-targeted therapeutic strategies for PDAC.

Brookens SK, DeGaramo DA, Wilson K et al. · Cancer research · (2026) · View on PubMed ↗

EP300-Mediated MTF1-K218 Lactylation Buffers AR-Driven Copper Overload to Suppress Cuproptosis in Castration-Resistant Prostate Cancer.

The authors studied how EP300-mediated MTF1-K218 lactylation affects androgen receptor (AR)–driven copper handling in castration-resistant prostate cancer (CRPC). They found that AR hyperactivation increases copper uptake while MTF1-dependent lactylation buffers copper toxicity, suppressing physiological cuproptosis despite elevated tumor copper. Clinically, this defines an EP300–MTF1 lactylation axis as a potential vulnerability to overcome copper-buffering and sensitize CRPC to cuproptosis-based therapies.

Li K, Wei Y, Li Y et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Generation of Nasal Cell-Derived Human Alveolar Organoids and Organoid-Macrophage Assembloids for in Vitro Lung Modeling.

The study generated nasal cell-derived human alveolar organoids (nsoAlvO) and peripheral blood monocyte-derived alveolar macrophages (monoAM), then created organoid–macrophage assembloids to model lung epithelial–immune interactions in vitro. Co-culture enhanced maturation of both components, and single-cell RNA sequencing plus immunostaining and functional assays showed that the assembloids phenocopied native alveolar epithelium and macrophage states with dynamic epithelial–macrophage communication. This platform enables physiologically relevant lung modeling and provides a scalable system for studying alveolar biology and testing immunotherapies.

Chiu MC, Zhang S, Li C et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗


Neurodegeneration, Neuroinflammation & Brain Aging

Association Between Menopausal Hormone Therapy and Alzheimer Disease Neuropathology.

This cohort study examined whether estrogen-only menopausal hormone therapy (MHT) is associated with Alzheimer disease (AD) neuropathology, clinical outcomes, and imaging/fluid biomarkers in women using two large datasets (NACC and ADNI). The key finding is that the study was designed to test associations between estrogen-only MHT exposure and dementia/AD biomarker endpoints across these independent cohorts (specific results are not included in the provided abstract text). Scientifically, it addresses how menopausal estrogen decline and hormone exposure may influence AD pathogenesis by linking MHT to neuropathologic and biomarker measures rather than only clinical diagnosis.

Bruno J, Shaw JS, Hosseini SMH · Neurology · (2026) · View on PubMed ↗

Blood SOD1 Activity in ALS Patients Receiving Tofersen Treatment.

The study measured blood SOD1 enzymatic activity in ALS patients receiving the antisense oligonucleotide tofersen, using a discovery cohort (n=120) and validation cohort (n=208) including controls and sporadic ALS (sALS) patients. The key finding was that tofersen treatment was associated with measurable changes in blood SOD1 activity, addressing a previously unclear pharmacodynamic effect relevant to SOD1 biology. Monitoring SOD1 activity may help assess therapeutic impact and safety in SOD1-related ALS where reduced activity is linked to severe motor neuron impairment.

Goehring K, Abler E, Vavra J et al. · Annals of neurology · (2026) · View on PubMed ↗

Plasticity of human microglia and brain perivascular macrophages in aging and Alzheimer’s disease.

The study profiled 832,505 human myeloid cells from the prefrontal cortex of 1,607 donors across the lifespan with varying Alzheimer’s disease (AD) neuropathology to define microglial and brain perivascular macrophage states. It identified a disease-associated microglial subtype with elevated GPNMB expression and enriched polygenic AD risk that expands with AD pathology and shows increased phagocytic activity, and it implicated MITF in this program. These findings improve mechanistic understanding of AD-associated myeloid plasticity and nominate GPNMB/MITF-linked pathways as potential targets.

Lee D, Vicari JM, Porras C et al. · Nature genetics · (2026) · View on PubMed ↗

Oxidative stress and inflammation in neurodegenerative disorders.

This review studied the role of oxidative stress and inflammation across neurodegenerative disorders including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. It highlights how mitochondrial and metal-associated processes (e.g., amyloid-beta binding to iron/copper) promote reactive oxygen species (ROS) generation, membrane peroxidation, and downstream neuronal death, linking oxidative damage to hallmark pathologies such as amyloid-beta plaques and hyperphosphorylated tau aggregates. The synthesis underscores oxidative stress as a unifying pathogenic driver and supports antioxidant/anti-inflammatory strategies as potential therapeutic avenues.

Jomova K, Alomar SY, Valko R et al. · Archives of toxicology · (2026) · View on PubMed ↗

GLP-1 receptor agonists, metabolic syndrome, and Alzheimer’s disease: Lessons and opportunities from the EVOKE trials.

This review synthesized evidence from the EVOKE trials and related data to examine whether glucagon-like peptide-1 receptor agonists (GLP-1RAs) can influence Alzheimer’s disease (AD) risk or AD-related pathways in metabolically vulnerable populations with metabolic syndrome. The key conclusion was that shared mechanisms—vascular injury, insulin resistance, and chronic inflammation—provide a rationale for GLP-1RA effects on neurodegenerative processes and potential risk modification. This is important for guiding future trials testing GLP-1RAs as disease-modifying or risk-reducing therapies for AD in patients with metabolic syndrome.

Gupta P, Pozzilli V, De Giovanni A et al. · Journal of neuroendocrinology · (2026) · View on PubMed ↗

Senescent microglia with shortened telomeres secrete soluble DLK1 to induce aging-associated hypomyelination and neuronal dysfunction.

This work studied telomere-shortened mice and human iPSC-derived microglia senescence models to determine how senescent microglia drive aging-associated brain changes. Single-nucleus RNA-seq showed accelerated glial aging and microglial senescence pathways, and the authors identified soluble delta-like non-canonical Notch ligand 1 (sDLK1) as a senescence-associated ligand that increased in cerebrospinal fluid and induced hypomyelination and neuronal dysfunction. The results implicate DLK1-mediated signaling from senescent microglia as a mechanistic link between telomere attrition and neurodegeneration-relevant phenotypes.

Liu B, Mahoney M, Feng Y et al. · Neuron · (2026) · View on PubMed ↗

A Small-Molecule DEPTAC Rescues Cognitive Deficits by Targeted Dephosphorylation of Pathological Tau.

The study developed TP2, a small-molecule DEPTAC that tethers endogenous PP2A to pathological tau, and tested whether targeted dephosphorylation of Tau reduces neurodegeneration in tauopathy mouse models expressing P301L or AAV-hTau-N368. TP2 formed a ternary complex with PP2A and Tau, potently reduced neuronal p-Tau, oligomers, and neurofibrillary tangles after systemic TP2 dosing, and did so without altering global PP2A activity. This suggests a precision pharmacology approach for Alzheimer’s disease by directly targeting pathological Tau phosphorylation rather than broadly modulating phosphatases.

Sun F, Liu Y, Zhou Q et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗


Neurobiology & Neural Circuitry

Multimerization of ELAV in Drosophila is essential for directing neuronal alternative splicing and polyadenylation programs.

This study investigated how the ELAV/Hu family RNA-binding protein ELAV regulates neuronal alternative splicing and polyadenylation in Drosophila photoreceptor neurons, focusing on ELAV multimerization. X-ray crystal structures of ELAV RRM3 showed that multimerization forms a tetramer via two conserved interfaces in non-RNA-binding regions, and mutational probing demonstrated that both interfaces are required for ELAV function in development. The work clarifies a mechanism by which ELAV achieves gene-specific regulation through protein multimerization, advancing understanding of neuronal transcriptome control.

Dix TC, McQuarrie DWJ, Bräuer U et al. · Genes & development · (2026) · View on PubMed ↗

Approaching a connectome of the human foveal retina.

The study constructed a working-draft connectome of the human foveal retina by using deep learning to segment cells and synaptic connections in a piece of human foveal tissue. It classified ~3,000 cells into 51 neuronal types and three glial types and mapped synaptic motifs, including midget and small bistratified ganglion cell circuits. This high-resolution human connectome resource advances circuit-level understanding of foveal processing and supports future targeted neuroscience and disease modeling.

Kim YJ, Packer O, Macrina T et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗


Cardiovascular Disease & Cardiac Remodeling

Disease modifying treatment of hereditary transthyretin amyloidosis with polyneuropathy in Germany - expert consensus of the German society of amyloid diseases (DGAK) and the German neurological society (DGN).

The article provided an expert consensus on disease-modifying treatment for hereditary transthyretin amyloidosis with polyneuropathy (ATTRv-PN) in Germany, focusing on the transthyretin (TTR) gene and two therapeutic classes: TTR stabilizers and gene silencers. Across trials, disease progression was significantly slowed and patients’ span and quality of life improved versus placebo, even though lost function was not fully recovered. This consensus supports evidence-based selection and implementation of DMT strategies for ATTRv-PN patients in clinical practice.

Weiler M, Dohrn MF, Gingele S et al. · Neurological research and practice · (2026) · View on PubMed ↗

Vitronectin-driven amyloid deposition disrupts mitochondrial homeostasis via integrin-mediated pathway in a humanized mouse model of transthyretin cardiac amyloidosis.

This study used humanized knock-in mice expressing either wild-type transthyretin (hTTRWT) or the V142I mutant (hTTRV142I) to test whether vitronectin (VTN)-driven amyloid deposition disrupts mitochondrial homeostasis via an integrin-mediated pathway in transthyretin cardiac amyloidosis. The work assessed amyloid burden and cardiac dysfunction using Congo red staining, electron microscopy, echocardiography, and cardiac magnetic resonance, linking VTN/amyloid deposition to mitochondrial dysregulation through integrin signaling. If confirmed, targeting the VTN–integrin axis could represent a mechanistic therapeutic approach to preserve mitochondrial function and slow ATTR cardiac amyloidosis progression.

Qiu Z, Fan Y, Qin J et al. · European heart journal · (2026) · View on PubMed ↗

RUNX1-driven endothelial-to-mesenchymal transition contributes to remodelling in LMNA cardiomyopathy.

This study examined mechanisms of fibrotic remodeling in LMNA-related dilated cardiomyopathy by testing whether RUNX1-driven endothelial-to-mesenchymal transition (EndMT) contributes to remodeling. Using spatial transcriptomics and integrated single-nuclei multiomics on explanted human LMNA-DCM hearts, and then validating with patient-specific iPSC-derived endothelial cells, engineered cardiac organoids, and an LMNA model (details truncated), it identified endothelial transcriptional/epigenomic states linked to fibrosis and implicated RUNX1-driven EndMT as a contributor. These results support RUNX1-mediated EndMT as a potential therapeutic target to reduce fibrosis and progression in LMNA cardiomyopathy.

Wu D, Tripathi D, Manhas A et al. · European heart journal · (2026) · View on PubMed ↗


Renal Disease, Transplantation & Kidney Injury

Nonhistone Post-translational Modifications as Integrative Signaling Networks in Podocyte Injury and Glomerular Disease.

This article reviewed how nonhistone post-translational modifications act as integrative signaling networks in podocyte injury and glomerular disease. It emphasizes that, beyond histone marks, nonhistone PTMs regulate protein stability, activity, localization, and interactions that drive podocyte dysfunction and proteinuria. The synthesis highlights mechanistic PTM pathways as potential biomarkers and therapeutic targets for chronic glomerular disorders.

He Z, Jiang H, Tao S et al. · Journal of the American Society of Nephrology : JASN · (2026) · View on PubMed ↗

Real-world modality selection and outcomes in neonatal kidney replacement therapy: a single-center cohort study.

This single-center retrospective cohort study compared peritoneal dialysis (PD), continuous kidney replacement therapy (CKRT), and sequential PD+CKRT in neonates requiring kidney replacement therapy, analyzing biochemical response, complications, and mortality predictors. PD patients had lower gestational age and birth weight than CKRT patients, and the study evaluated modality-associated outcomes and factors linked to death. The scientific significance is that it informs real-world modality selection for neonatal KRT by identifying outcome differences and mortality correlates across PD versus CKRT strategies.

Demirtaş F, Aghayeva S, Aplak B et al. · European journal of pediatrics · (2026) · View on PubMed ↗

Management of Recurrent C3 Glomerulopathy After Kidney Transplantation.

This review article focused on recurrent C3 glomerulopathy (C3G) after kidney transplantation, a complement-mediated ultra-rare glomerular disease with a high risk of early post-transplant recurrence. It highlights that improved histopathologic recognition and increased use of protocol biopsies show C3G often recurs early and frequently subclinically, while no validated clinical, genetic, or functional biomarkers currently predict recurrence reliably. Clinically, this underscores the need for better predictive biomarkers and surveillance strategies to prevent graft dysfunction and loss from recurrent C3G.

Trujillo H, Cavero T, Moran SM et al. · Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · (2026) · View on PubMed ↗ · Free PDF ↗


Hepatology, Liver Disease & Metabolic Liver Disorders

Multi-omics dissection of MASLD reveals divergent pathways to systemic diseases and targets for prevention.

This study performed a genome-wide association study (GWAS) using MRI-derived hepatic fat content in 33,592 UK Biobank participants to define genetically distinct metabolic dysfunction-associated steatotic liver disease (MASLD) subtypes and link them to extrahepatic systemic disease risk. Clustering of MASLD-associated SNPs with triglyceride-related traits identified divergent MASLD genetic subtypes and highlighted protein-mediated mechanisms as potential prevention targets. These multi-omics, genetics-driven MASLD stratifications could enable subtype-specific risk prediction and preventive interventions for systemic complications.

Weng Y, Du M, Wu T et al. · Metabolism: clinical and experimental · (2026) · View on PubMed ↗

Targeting the E3 ubiquitin ligase RNF10 ameliorates metabolic dysfunction-associated steatohepatitis in mice.

This study examined the role of the E3 ubiquitin ligase RNF10 in metabolic dysfunction-associated steatohepatitis (MASLD) using mouse models and human correlation analyses. Hepatic-specific Rnf10 deletion reduced steatosis, inflammation, and fibrosis, whereas AAV-mediated hepatic Rnf10 overexpression worsened MASLD phenotypes, with RNF10 promoting CPT1A degradation via K48-linked ubiquitination. These results position RNF10 as a therapeutic target to restore fatty-acid oxidation and ameliorate MASLD progression.

Du C, Zhang Y, Chang H et al. · The Journal of clinical investigation · (2026) · View on PubMed ↗

Hepatocyte-intrinsic ER stress and NRF2 initiate primary sclerosing cholangitis, providing therapeutic insights.

The study investigated how hepatocyte-intrinsic ER stress and oxidative stress activate NRF2 and whether this combination initiates primary sclerosing cholangitis (PSC) in mice, including genetically affected animals and mice treated with an ER stress inducer plus an NRF2 activator. The combined stressors drove NRF2 activation in both hepatocytes and cholangiocytes and led to PSC with human-like features, recapitulating disease progression in experimental models. This provides a gene-regulatory mechanism (NRF2 downstream of ER/oxidative stress) and a potential therapeutic entry point for PSC.

Tao L, He P, Ge J et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗


Pulmonary Disease, Lung Injury & Pulmonary Immunology

Glutaminase regulates alveolar regeneration through autophagy-YAP/TAZ in pulmonary fibrosis.

This study examined how glutaminase 1 (GLS1)-dependent glutamine metabolism regulates alveolar regeneration through autophagy and YAP/TAZ signaling in pulmonary fibrosis. The key finding is that the authors used primary murine AT2 cells, alveolar organoids, and lineage-tracing in bleomycin-induced lung injury models to determine the role of AT2-specific GLS1 deletion in AT2-to-AT1 differentiation and regeneration (full results are truncated). Scientifically, it connects metabolic control (GLS1), autophagy, and mechanotransduction (YAP/TAZ) to lung repair mechanisms, suggesting potential metabolic targets to promote regeneration in fibrosis.

Pantuck MA, Zhang X, Meshkini F et al. · American journal of respiratory cell and molecular biology · (2026) · View on PubMed ↗

AAV-NRF2 protects retinal and choroidal vasculature in a GDF15-dependent manner in an oxidative damage model of AMD.

The study tested whether AAV-mediated overexpression of the antioxidant transcription factor NRF2 protects retinal and choroidal vasculature in NaIO3-induced oxidative damage (a dry AMD mouse model) and whether this protection depends on GDF15. AAV-NRF2 preserved deep retinal vascular plexus integrity, reduced choriocapillaris capillary disorganization/death, and mitigated electroretinographic decline in a GDF15-dependent manner. These findings support an AAV-NRF2/GDF15 axis as a mechanistic therapeutic strategy to prevent early vascular injury in AMD.

Wang S, Zhao S, Daniels A et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗


Autoimmunity, Inflammation & Immune Regulation

Succinate drives macrophage inflammation by promoting GPR91 mitochondrial signaling in rheumatoid arthritis.

This study investigated how succinate drives macrophage inflammation through GPR91 mitochondrial signaling in rheumatoid arthritis (RA), focusing on concentration-dependent and biphasic effects of succinate on GPR91. The key finding is that at physiological succinate levels, membrane-localized GPR91 promotes M2 polarization via Gq-mediated phospholipase C activation and intracellular calcium mobilization, whereas in RA elevated succinate induces GPR91 internalization and mitochondrial translocation. These mechanistic insights support GPR91 as a potential therapeutic target but suggest that dosing/ligand concentration and subcellular localization may determine whether signaling is pro- or anti-inflammatory.

Zhang W, Wang L, Zhao Y et al. · Science translational medicine · (2026) · View on PubMed ↗

Impact of Prior Biologic Mechanism of Action on Anti-TNF Effectiveness in Inflammatory Bowel Disease: An ENEIDA Registry Study.

This ENEIDA registry study evaluated whether the prior biologic mechanism of action (MOA) affects the effectiveness and durability of subsequent anti-TNF therapy in inflammatory bowel disease (IBD). The key finding is that, using propensity score matching, the study compared outcomes of second-line anti-TNF after a first biologic with a different MOA versus matched controls receiving second-line anti-TNF after another anti-TNF (specific effectiveness results are truncated in the provided abstract). Clinically, it addresses treatment sequencing by identifying whether prior MOA influences anti-TNF durability for active luminal disease.

Yagüe Caballero C, García López S, Royo Esteban A et al. · Alimentary pharmacology & therapeutics · (2026) · View on PubMed ↗

Innate immunity: current understandings and future perspectives.

This review summarized current understandings and future perspectives on innate immunity, emphasizing germline-encoded pattern recognition receptors (PRRs) that detect pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs). It highlighted how PRR signaling pathways converge on cytokine production and inflammasome activation. The synthesis is significant for guiding future research and therapeutic targeting of innate immune pathways in infection, inflammation, and tissue injury.

Zou C, Ma T, Li J et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗

TIF1γ regulates stability of regulatory T cells during inflammation.

This study examined how transcriptional intermediary factor 1-γ (TIF1γ) regulates regulatory T (Treg) cell stability in mouse models during inflammatory challenge. TIF1γ-deficient Treg cells lost Foxp3 and acquired effector phenotypes in a cell-intrinsic manner, adopting type 1 helper T–like or pro-inflammatory ex-Treg states in autoimmune settings and type 2 helper T–like features during helminth infection. These findings identify TIF1γ as a key molecular determinant of Treg lineage stability, with implications for understanding and potentially targeting Treg dysfunction in autoimmunity and infection.

Contreras-Castillo E, Zambrano-Romero JD, Núñez-Martínez HN et al. · Nature immunology · (2026) · View on PubMed ↗

PA200 modulates immunoproteasome structure and activity.

This study examined how the proteasome activator PA200 modulates immunoproteasome (i20S) structure and activity compared with the standard proteasome (s20S) using cryo-EM and in vitro biochemical assays. Cryo-EM structures of singly- and doubly-capped i20S–PA200 complexes showed that initial PA200 binding induces allosteric bending of i20S and widens the opposite α-ring, increasing PA200 occupancy and strengthening activation relative to s20S, while also shifting cleavage specificity toward caspase-like activity. These mechanistic insights clarify how PA200 selectively tunes immunoproteasome proteolysis, informing strategies to modulate antigen processing and immune responses.

Živković D, Bosc-Rosati A, Dafun AS et al. · Nature communications · (2026) · View on PubMed ↗

High-sensitivity flow cytometry in rheumatoid arthritis shows that early B-cell subset depletion is linked to 5-year rituximab response, while failure to deplete B cells occurs early in subsequent poly-refractory disease.

This study assessed whether early B-cell subset depletion measured by high-sensitivity flow cytometry (HSFC) predicts rituximab (RTX) response in rheumatoid arthritis (RA) and how this changes across disease refractoriness. In a single-center real-world cohort of 232 RTX-treated RA adults, complete depletion of naïve and memory B cells and plasmablasts at baseline and 2 weeks (2W) was defined as counts <0.1 cells/µL, and the study linked early depletion patterns to 5-year RTX response while showing that failure to deplete B cells emerged early in subsequent poly-refractory disease. These results suggest HSFC-based early B-cell depletion as a biomarker for long-term RTX responsiveness and for identifying patients likely to become refractory.

Tonutti A, Abacar K, David P et al. · Annals of the rheumatic diseases · (2026) · View on PubMed ↗

Neutralising autoantibodies against IL-10 and HLA-DRB1*01:03 in paediatric patients with inflammatory bowel disease.

This cross-sectional multicentre study assessed prevalence and clinical phenotype of neutralising autoantibodies against interleukin-10 (anti-IL-10) in paediatric inflammatory bowel disease (IBD) patients (mean IBD onset 11.2±3.8 years) and evaluated association with HLA-DRB101:03. Anti-IL-10 positivity was investigated in serum/plasma and was reported to be associated with carriage of the HLA-DRB101:03 allele. These findings support a genetically linked, immune-mediated subgroup of paediatric IBD that may inform future stratification and targeted immunological therapies.

Gharahdaghi N, Yeh PJ, Vadakethala K et al. · Gut · (2026) · View on PubMed ↗

The genesis of cutaneous neurogenic inflammation is a multi-step process requiring dendritic cell aggregation.

The study investigated how cutaneous neurogenic inflammation is initiated using optogenetic activation of TRPV1-expressing nociceptors to induce type-17 inflammation and examined the requirement for dendritic cell aggregation. Two rounds of nociceptor activation were required for maximal Il1b and Il6 expression and for Il23a induction, with transient type 2 dendritic cell (DC2) aggregation depending on substance P–Mrgprb2-dependent mast cell activation and mast cell-derived CCL2. These findings define a multi-step neuroimmune pathway that could be targeted to prevent or treat type-17–driven inflammatory skin disease.

Chen CS, Gillis JE, Cohen JA et al. · Immunity · (2026) · View on PubMed ↗

Use of Fluid Biomarkers in NMOSD and MOGAD: Clinical and Research Applications.

This 2026 review synthesized clinical and research evidence on the use of fluid biomarkers—AQP4-IgG and MOG-IgG—in neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). The key finding was that these biomarkers transformed disease classification by enabling antibody-defined subgroups, but optimal interpretation depends on integrating clinical and radiologic context. Scientifically and clinically, the review supports more accurate diagnosis and targeted therapy development for NMOSD/MOGAD based on biomarker status.

Mariotto S, Cobo-Calvo A, Khalil M et al. · Neurology(R) neuroimmunology & neuroinflammation · (2026) · View on PubMed ↗

Accuracy of Antibody Testing in Myasthenia Gravis: The ADAM Study.

The ADAM study prospectively compared diagnostic accuracy for acetylcholine receptor (AChR) and muscle-specific kinase (MuSK) autoantibodies in consecutive adult and pediatric patients with suspected myasthenia gravis across four Italian centers. The key finding was that different antibody-testing platforms—an in-house live cell-based assay (L-CBA), a fixed cell-based assay (F-CBA), and an indirect ELISA—showed varying diagnostic performance for AChR and MuSK detection in real-world practice. This is significant because it guides clinicians on which assay to use for accurate MG diagnosis, including in both adults and children.

Giannoccaro MP, Serra L, Grondona AG et al. · Neurology · (2026) · View on PubMed ↗

Targeting CXCR2 in Nociceptive Sensory Neurons Offers Novel Therapeutic Potentials for Postoperative Pain.

This study investigated postoperative pain mechanisms in a mouse skin-plus-deep tissue incision model by identifying CXCL5 upregulation and testing CXCL5/CXCR2 targeting, with single-cell RNA-seq support for CXCL5 expression in human skin wounds. Neutralizing CXCL5 abrogated incision pain, while global CXCR2 knockout improved pain but delayed wound healing; importantly, CXCR2 conditional knockout in nociceptive sensory neurons improved pain without affecting wound healing or local inflammation. The findings are clinically significant because they suggest CXCR2 inhibition limited to nociceptive sensory neurons could treat postoperative pain while preserving tissue repair.

Pan Y, Li P, Chen Y et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Impact of Biologic Therapies on the Risk of Progression from Psoriasis to Psoriatic Arthritis: A Systematic Review and Meta-Analysis of Cohort Studies.

This systematic review and meta-analysis evaluated cohort studies of adults with psoriasis without prior psoriatic arthritis to determine whether biologic therapies reduce the risk of incident psoriatic arthritis. Across included studies, biologic treatment was assessed for association with progression risk, using adjusted risk estimates to synthesize evidence on incident psoriatic arthritis outcomes. The results are significant for clinical decision-making because they inform whether biologics not only control skin disease but also modify downstream joint risk.

Xie W, Chen T, Chen Y et al. · American journal of clinical dermatology · (2026) · View on PubMed ↗


Infectious Disease & Host-Pathogen Interactions

Loss of cellular RNA homeostasis contributes to MDA5 activation during virus infection.

This study investigated what RNA ligands activate the innate immune sensor MDA5 during virus infection, using single-nucleotide resolution iCLIP (single-nucleotide resolution crosslinking and immunoprecipitation). After SARS-CoV-2 or encephalomyocarditis virus infection, MDA5 bound predominantly to cellular RNAs, with iCLIP peaks enriched in intronic regions near Alu elements and base-paired structures, alongside increased cytoplasmic aberrant and unspliced intron-containing transcripts. The results link loss of cellular RNA homeostasis to MDA5 activation, advancing mechanistic understanding of antiviral sensing and potential therapeutic modulation of MDA5-driven inflammation.

Sampaio NG, Davis T, Gearing LJ et al. · Nature immunology · (2026) · View on PubMed ↗

Convergent evolution of metabolic regulation governs redox adaptation in Toxoplasma.

Researchers screened the apicomplexan parasite Toxoplasma gondii to identify genes required for fitness during crowding, focusing on metabolic regulation under oxidative stress and nutrient/waste stress. They found that NAD(P)+ biosynthesis is required at high parasite density and identified an RNA-binding protein, TgPRO (T. gondii parasite response to oxidation), whose loss increased reactive oxygen species and impaired crowding adaptation. These mechanistic insights reveal conserved metabolic and redox adaptation dependencies that could be exploited for anti-toxoplasma strategies.

Giuliano CJ, Kalluraya CA, Kloehn J et al. · Cell · (2026) · View on PubMed ↗

Dysregulated BCR repertoire and metabolic state of HBsAg-specific B cells in chronic hepatitis B revealed by integrated single-cell analysis.

This work profiled HBsAg-specific B cells from HBeAg-positive chronic hepatitis B patients, convalescent individuals, and vaccinated healthy controls using integrated single-cell RNA sequencing (scRNA-seq) and single-cell B cell receptor sequencing (scBCR-seq). It found dysregulated BCR repertoires and altered metabolic states in HBsAg-specific B cells in chronic infection, with key observations validated in an independent cohort and recombinant monoclonal antibodies generated for functional testing. The results clarify how chronic HBV shapes B-cell receptor diversity and metabolism, informing strategies to improve humoral targeting of HBsAg for viral clearance.

He M, Shen L, Li Y et al. · Hepatology communications · (2026) · View on PubMed ↗

Influenza A(H1N1) triggered atypical hemolytic uremic syndrome in a child with homozygous CD46 variant successfully treated with ravulizumab: a case report.

This case report described a 12-year-old girl with influenza A(H1N1)–triggered atypical hemolytic uremic syndrome (aHUS) who had a homozygous pathogenic variant in CD46 and was successfully treated with ravulizumab. The patient presented with fever, diarrhea, abdominal pain, mucosal bleeding, jaundice, and acute kidney injury, with microangiopathic hemolytic anemia and thrombocytopenia and preserved ADAMTS13 activity, while viral testing confirmed H1N1. The clinical significance is that it supports ravulizumab as an effective treatment strategy for complement-mediated aHUS in patients with CD46 genetic susceptibility after influenza triggers.

Mazzillo Vega L, Montero Zambrano AC, Luna Mazzillo A · CEN case reports · (2026) · View on PubMed ↗

Helicobacter pylori eradication therapy and clinical outcomes in Parkinson’s disease: a double-blind randomized placebo-controlled trial.

This double-blind randomized placebo-controlled trial tested whether Helicobacter pylori eradication therapy improves Parkinson’s disease outcomes in H. pylori–positive adults. Participants received standard triple therapy (omeprazole 20 mg, amoxicillin 1000 mg, clarithromycin 500 mg twice daily for 14 days) versus matched placebo, with primary assessment using the MDS-UPDRS Part III motor score. The clinical significance is that it directly evaluates whether targeting H. pylori infection can modify motor and non-motor symptoms and quality of life in Parkinson’s disease.

Vishwas G, Kakkar AK, Mehta S et al. · Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · (2026) · View on PubMed ↗


Metabolism, Obesity & Endocrine Control

Pangenome-guided breeding restores high-altitude adaptation and improves yield in Tartary buckwheat.

This study generated a telomere-to-telomere reference genome and a 16-accession pangenome for Tartary buckwheat to uncover genes and superior alleles for high-altitude adaptation and yield. Graph-based pangenome analysis identified FtRNH, a wild-specific gene that enhances high-altitude adaptability, alongside extensive structural variation including gene copy-number variations across accessions. The pangenome-guided breeding targets provide actionable genetic resources to improve high-altitude crop performance.

Zhang K, He Y, Lin H et al. · Cell · (2026) · View on PubMed ↗

The sex and reproductive plasticity of intestinal muscles instruct gut size.

The authors studied how intestinal muscle controls gut size in Drosophila by comparing sex- and reproduction-dependent differences in intestinal muscle structure and growth. They showed that extrinsic muscle cues determine adult gut size, and that altering sex or reproductive status of gut muscle cells changes baseline sex differences in muscle myofibril width and organ size. This establishes intestinal muscle as a plastic, hormone- and nutrition-responsive instructive tissue for organ scaling.

Mineo A, Blackie L, Milona A et al. · Cell · (2026) · View on PubMed ↗

A nutrient-sensitive enterokine coordinates developmental plasticity through inter-organ signaling.

The study investigated nutrient-sensitive developmental plasticity in Drosophila larvae by identifying an endocrine enterokine mechanism coordinating inter-organ signaling under amino-acid restriction. It identified Limostatin, produced by a subset of larval midgut enteroendocrine cells, as a systemic inhibitor of dIlp2 expression/release, thereby slowing developmental progression when nutrients are limited. This mechanistic endocrine link between gut nutrient sensing and insulin-like developmental control highlights a conserved strategy for tuning growth to environmental conditions.

Bai L, Montagne J, Ramos CI et al. · PLoS biology · (2026) · View on PubMed ↗

Stearoyl-CoA desaturases regulate intestinal stem and progenitor cell metabolism and function in response to nutrient abundance.

Researchers studied how stearoyl-CoA desaturases SCD1 and SCD2 regulate intestinal stem/progenitor metabolism and function in response to nutrient abundance using intestinal mouse organoids and in vivo intestine-specific gene deletions. Pharmacologic inhibition or genetic deletion of Scd1/Scd2 disrupted lipid desaturation, induced ER stress, and impaired stem/progenitor proliferation, with oleic acid supplementation largely rescuing the defects; in vivo, Scd1/Scd2 deletion reduced LGR5+ stem cells and drove metabolic rewiring. The findings link SCD-dependent lipid desaturation to intestinal homeostasis and suggest metabolic modulation of SCD activity as a lever for stem-cell maintenance.

Akkaya-Colak KB, Keller AR, Festing MH et al. · Cell reports · (2026) · View on PubMed ↗

Microbiota-derived isovalerate ameliorates sex-specific gut barrier dysfunction in malnutrition.

The study tested whether microbiota-derived isovalerate can ameliorate sex-specific gut barrier dysfunction in malnutrition using SPF and germ-free mouse models of low-protein, low-fat diet malnutrition. It quantified colonic permeability in Ussing chambers, cultured invasive bacteria from liver and spleen, and used targeted metabolomics to identify metabolites depleted in malnutrition, then screened candidate metabolites in human-derived colonoid monolayers. The work supports a microbiome-metabolite mechanism—specifically isovalerate—that can restore gut barrier function and reduce infection risk in malnourished hosts, with effects differing by sex.

Lynch LE, Soni KG, Spinler JK et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Inhibiting menin attenuates high-fat diet-induced weight gain by limiting intestinal lipid absorption in mice.

The study tested whether inhibiting menin (Men1) in intestinal epithelial cells limits high-fat diet-induced obesity by altering lipid absorption and intracellular triglyceride handling in mice. IEC-specific Men1 knockout protected against high-fat diet weight gain and increased CES1 expression, which promoted triglyceride hydrolysis and reduced intracellular TG storage, thereby limiting ApoB48-dependent lipid transport. These findings position the menin–CES1 pathway as a potential target to reduce intestinal lipid absorption and treat obesity.

Cao X, Zhou P, Meng H et al. · The Journal of clinical investigation · (2026) · View on PubMed ↗

Sex- and Trimester-Specific Associations of Prenatal Co-Exposure to Organophosphate Esters and Phthalates with Preschoolers’ Trajectories of Co-Occurring ADHD and ASD Symptoms: Cord Blood Metabolomic Study in the Ma’anshan Birth Cohort.

Using cord blood metabolomic data from 3040 mother–child dyads in the Ma’anshan Birth Cohort, this study examined sex- and trimester-specific associations between prenatal co-exposure to organophosphate esters (OPEs) and phthalates (PAEs) and preschool trajectories of co-occurring ADHD and ASD symptoms. Group-based multitrajectory modeling and single-pollutant models identified trimester-dependent associations for specific chemicals such as bis(2-ethylhexyl) phosphate (BEHP) with symptom cotrajectories, with metabolic mechanisms proposed via metabolomic profiling. This is significant because it links specific prenatal endocrine-disrupting exposures and metabolic signatures to neurodevelopmental risk patterns that may differ by sex and pregnancy timing.

Wang X, Tong J, Lu M et al. · Environmental science & technology · (2026) · View on PubMed ↗


Clinical Trials, Guidelines & Real-World Evidence

Belzutifan plus lenvatinib versus cabozantinib in patients with previously treated advanced renal cell carcinoma (LITESPARK-011): an open-label, randomised, controlled, phase 3 trial.

This phase 3, open-label randomized trial studied belzutifan plus lenvatinib versus cabozantinib in adults with previously treated advanced clear-cell renal cell carcinoma after immune checkpoint inhibitor therapy (LITESPARK-011; 184 centers across 25 countries). The key finding reported in the abstract is that the study was designed to establish a post–anti–PD-1/PD-L1 treatment standard of care by comparing efficacy and safety between these regimens, with outcomes including overall survival and progression-free survival (details truncated in the provided text). Clinically, the trial directly targets an unmet need for optimal sequencing after checkpoint inhibitors in advanced clear-cell RCC by testing a hypoxia/HIF-2α pathway inhibitor (belzutifan) combined with VEGFR/RTK inhibition (lenvatinib) against cabozantinib.

Motzer RJ, McDermott R, Park SH et al. · Lancet (London, England) · (2026) · View on PubMed ↗

Risk Reclassification Beyond BMI by Waist Circumference and Waist-to-Hip Ratio Across 9 Cardiovascular Outcomes: Results From the Cross-Cohort Collaboration.

This cross-cohort collaboration study assessed whether central adiposity measures—waist circumference (WC) and waist-to-hip ratio (WHR)—improve cardiovascular disease (CVD) risk reclassification beyond BMI across nine cardiovascular outcomes. The key finding is that the analysis quantified how many individuals are reclassified or misclassified when using WC/WHR compared with BMI-based normal/overweight/obesity categories, and evaluated the prognostic implications for CVD risk (numerical results are truncated in the provided abstract). Scientifically and clinically, it suggests that incorporating central fat distribution metrics may better stratify CVD risk than BMI alone, especially when BMI categories are discordant with body composition.

Dardari ZA, Yao Z, Zhang J et al. · Journal of the American College of Cardiology · (2026) · View on PubMed ↗

Placenta Accreta Spectrum: A Narrative Review of Clinical Management, Contemporary Innovations, And Global Challenges.

This narrative review synthesized current clinical management and emerging innovations for placenta accreta spectrum (PAS), emphasizing challenges in translating high-resource diagnostic and multidisciplinary surgical frameworks to resource-limited settings. The key finding is the identification of knowledge gaps and the need for synthesized evidence on integrating emerging technologies (e.g., machine learning models and real-time intraoperative flow assessments) with traditional imaging to optimize surgical outcomes (specific comparative results are not provided because it is a review). Clinically, it highlights where future research and implementation efforts should focus to improve PAS diagnosis and outcomes globally, particularly where advanced imaging and multidisciplinary resources are limited.

Ezeigwe CO, Eleje GU, Eze UP et al. · International journal of medical science and dental health · (2026) · View on PubMed ↗

Outcomes of Cisplatin, Gemcitabine, and Durvalumab According to TOPAZ-1 Study Eligibility: A Large Global Analysis in a Real-World Setting.

This real-world, retrospective global analysis studied first-line cisplatin and gemcitabine plus durvalumab (CGD) in advanced biliary tract cancer (BTC) patients who were either eligible or ineligible for the TOPAZ-1 trial criteria (TOPAZ-1-in vs TOPAZ-1-out; 1358 patients across 55 centers). The key finding is that the study evaluated overall survival (OS), progression-free survival (PFS), objective response rate (ORR), disease control rate (DCR), and safety in these two groups to determine how TOPAZ-1 eligibility affects outcomes (numerical results are truncated). Clinically, it informs whether CGD benefits extend to broader real-world BTC populations that would otherwise be excluded from the pivotal trial.

Prinzi FL, Rimini M, Ikeda M et al. · International journal of cancer · (2026) · View on PubMed ↗

CREB promotes starvation-induced sleep loss by regulating octopamine production in Drosophila.

This Drosophila study investigated how the transcription factor CREB regulates starvation-induced sleep loss by controlling octopamine production. The key finding is that CREB is activated during starvation via the Sik2-CRTC pathway and promotes reduced sleep by upregulating tyramine β-hydroxylase (TβH), the rate-limiting enzyme for octopamine (OA) synthesis, with CREB-dependent effects on starvation-driven behavioral changes (details truncated). Scientifically, it links a conserved cAMP-responsive transcriptional program to neuromodulator biosynthesis, clarifying molecular circuitry underlying starvation-associated sleep disruption.

Zhu S, Rao Z, Yin Y et al. · Biology open · (2026) · View on PubMed ↗

Individualized Connectivity-Guided Versus Conventional Targeting of Accelerated Theta-Burst Stimulation in Depression: A Randomized, Double-Blind, Parallel-Design Trial.

This randomized, double-blind, parallel-design trial compared individualized connectivity-guided intermittent theta-burst stimulation (iTBS) versus conventional 5-cm targeting for scalp-based rTMS over the left dorsolateral prefrontal cortex (DLPFC) in adults with major depressive disorder or bipolar II depression. The key finding was that individualized connectivity-guided iTBS improved antidepressant outcomes compared with conventional 5-cm targeting. If confirmed, connectivity-guided robotic neuronavigation–based iTBS could increase response rates by accounting for interindividual variability in target connectivity.

Li M, Wu Z, Lu X et al. · The American journal of psychiatry · (2026) · View on PubMed ↗

UNCOVERseq enables sensitive and controlled gene editing off-target nomination across CRISPR-Cas modalities and systems.

This study developed and validated UNCOVERseq, an in cellulo workflow for sensitive and controlled CRISPR off-target nomination across CRISPR-Cas modalities and systems. Using enhanced RhPCR with defined inputs and process controls, UNCOVERseq achieved high analytical sensitivity (97.6%) and precision (78%) on an inter-method off-target confirmation benchmarking dataset, and it was applied across 192 guide RNAs to identify rare off-target events. The method improves off-target risk assessment for gene editing by providing more reliable nomination of candidate off-target variants for downstream confirmation.

Kinney KJ, Jia K, Zhang H et al. · Nature communications · (2026) · View on PubMed ↗

Association Between Metformin Use and Risk of Lung Cancer in Patients With Type 2 Diabetes: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis studied whether metformin use in adults with type 2 diabetes mellitus (T2DM) is associated with lung cancer risk. It pooled observational evidence from studies identified via database searches up to January 1, 2026, using the most fully adjusted hazard ratios (HRs) with 95% confidence intervals. The analysis aims to clarify whether metformin’s potential anticancer effects translate into reduced lung cancer incidence in real-world T2DM populations.

Karimi M, Hooshmand F, Mohammadian K et al. · Cancer reports (Hoboken, N.J.) · (2026) · View on PubMed ↗

Effectiveness, safety, and treatment persistence of bempedoic acid in a Spanish real-world cohort.

This retrospective multicenter study evaluated the effectiveness, safety, and treatment persistence of bempedoic acid (BA) in a Spanish real-world cohort of 814 patients with vascular risk. BA treatment was assessed by changes in lipid and laboratory parameters at baseline and after 3 months, using generalized mixed models to estimate adjusted marginal means and treatment persistence outcomes. The findings provide practical evidence for BA’s LDL-C–lowering benefit and tolerability in patients, particularly those with statin intolerance.

León-Jiménez D, Martínez-Hervás S, Lois-Martínez N et al. · Journal of clinical lipidology · (2026) · View on PubMed ↗

Real-world ADHD pharmacological treatment patterns and their association with negative clinical outcomes in youth with comorbid autism: a Swedish population-based study.

Using Swedish population-based real-world data, this study examined ADHD pharmacological treatment patterns (initiation timing, medication choice, switching, discontinuation) in youth with comorbid autism spectrum disorder (ADHD+ASD) versus youth with ADHD alone. The study assessed whether alternative ADHD medication choices and treatment trajectories were associated with negative clinical outcomes in this comorbidity context. These results are clinically relevant for optimizing real-world ADHD medication strategies in youth with ASD.

Garcia-Argibay M, Kuja-Halkola R, D’Onofrio BM et al. · BMJ mental health · (2026) · View on PubMed ↗

Evidence based interventions for bipolar disorder across phases and age groups: living umbrella review, evaluation, analysis, and communication hub (U-REACH) project.

The U-REACH project conducted a living umbrella review to evaluate the certainty of evidence for bipolar disorder treatment strategies across age groups and mood phases, and to build an open-access decision-support platform. It systematically synthesized evidence from network or pairwise meta-analyses of randomized controlled trials covering pharmacological, nutraceutical, psychosocial, brain stimulation, and circadian rhythm interventions. This is significant for improving evidence transparency and shared decision-making in bipolar disorder care across developmental stages and clinical phases.

De Prisco M, Oliva V, Miola A et al. · BMJ (Clinical research ed.) · (2026) · View on PubMed ↗

Competing risks of treatment discontinuation of atezolizumab plus bevacizumab in unresectable hepatocellular carcinoma.

In a multicentre retrospective cohort of 685 consecutive patients with unresectable hepatocellular carcinoma treated with atezolizumab plus bevacizumab (Atezo/Bev), this study quantified competing risks of treatment discontinuation and identified predictors. It characterized cause-specific discontinuation by separating discontinuation due to progressive disease versus adverse events and modeled time-varying probabilities of each cause. These findings are clinically significant because they refine understanding of why Atezo/Bev is stopped and can help anticipate and mitigate discontinuation drivers.

Suda G, Sho T, Abe T et al. · JHEP reports : innovation in hepatology · (2026) · View on PubMed ↗

Effects and underlying mechanisms of repeated low-level red light on refractive development in Guinea pigs with different refractive states.

This experimental study tested whether repeated low-level red light (RLRL) alters refractive development in guinea pigs with different baseline refractive states (myopia, hyperopia, and myopia recovery). Using lens-induced refractive error models and daily RLRL intervention, the key finding was that RLRL modulated refractive outcomes compared with controls, with mechanistic exploration reported in the truncated methods/results. The work is significant for developing non-pharmacologic, light-based strategies to influence refractive development and myopia progression.

Liu T, Li Z, Liu Q et al. · Experimental eye research · (2026) · View on PubMed ↗

Radiation Therapy for Pancreatic Cancer: An ASTRO Clinical Practice Guideline.

This ASTRO Clinical Practice Guideline reviewed evidence to provide recommendations for radiation therapy (RT) in pancreatic cancer across resectable, borderline resectable, locally advanced, metastatic, and symptomatic settings. The key output was guideline-based consensus on indications/timing, dose-fractionation, target volumes, and preferred planning/delivery techniques for nonmetastatic disease. Clinically, it standardizes RT decision-making and technical approaches to improve care consistency for pancreatic cancer patients.

Chuong MD, Jethwa KR, Ludmir E et al. · Practical radiation oncology · (2026) · View on PubMed ↗

Effectiveness of beta-blockers in COPD and CVD: Real-world effects on mortality.

Using the UK Clinical Practice Research Datalink (CPRD), this real-world cohort study evaluated whether initiating beta-blockers in patients with chronic obstructive pulmonary disease (COPD) and cardiovascular disease (CVD) reduces mortality and whether effects differ with concurrent long-acting β2-agonist bronchodilator (LABA) use. The study design used a prev/incident-user approach (truncated in the abstract) to estimate mortality associations and effect modification by LABA co-therapy. This is significant because it informs safety and effectiveness of beta-blockers in COPD patients with CVD in routine clinical practice.

Suissa S, Dell’Aniello S, Renoux C et al. · Chest · (2026) · View on PubMed ↗

Single-cell and bulk RNA-seq with machine learning reveals CCNB1/CDK1-mediated G2/M arrest as key anti-HCC mechanism of Fuzheng Xiaozheng Prescription.

This study evaluated the real-world impact of Turkey’s national newborn screening (NBS) program on survival and functional outcomes in infants with spinal muscular atrophy (SMA) type 1 who have two SMN2 copies and were treated with nusinersen. Compared with a historical pre-NBS symptomatic cohort (n=162), the NBS-identified cohort (n=96) showed improved clinical outcomes, supporting earlier diagnosis and treatment. The findings strengthen evidence that newborn screening plus nusinersen improves prognosis in genetically defined high-risk SMA.

Li X, Zhu B, Yang J et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗

Body region and clinical indication-based diagnostic reference levels for pediatric CT: Multicenter study from the MENA region.

This multicenter study collected retrospective and prospective CT dose data from 15,707 pediatric patients across 38 MENA sites to establish body region- and clinical indication-based diagnostic reference levels (DRLs) for pediatric CT. The key finding was that the dataset enabled region- and indication-specific DRL characterization for pediatric CT in the Middle East and North Africa, addressing a major evidence gap. These MENA-specific DRLs can support dose optimization and standardization for pediatric CT protocols in clinical practice and quality assurance across the region.

Karout L, Alkhazzam S, Kharita MH et al. · Journal of medical imaging and radiation sciences · (2026) · View on PubMed ↗

Chemotherapy type and survival in young BRCA1/2 carriers with HER2-negative early breast cancer.

This international retrospective cohort study (BRCA BCY Collaboration, NCT03673306) evaluated disease-free survival (DFS) and overall survival (OS) in young (≤40 years) germline BRCA1/BRCA2 pathogenic variant carriers with HER2-negative stage I–III early breast cancer treated with different (neo)adjuvant chemotherapy regimens. The key finding was that chemotherapy type (anthracycline-taxane vs anthracycline-no-taxane vs non-anthracycline) was associated with survival outcomes in this HER2-negative BRCA carrier population. Clinically, the results aim to inform (neo)adjuvant chemotherapy selection for young BRCA1/2 carriers when HER2 is negative, where evidence has been limited.

Bernstein-Molho R, Sella T, Delucchi V et al. · European journal of cancer (Oxford, England : 1990) · (2026) · View on PubMed ↗

Renal Outcomes of Triglyceride-Targeting Lipid-Lowering Therapies versus Statins in Patients with CKD.

This retrospective target trial emulation compared renal outcomes of triglyceride-targeting lipid-lowering therapies (e.g., fibrates and niacin) versus statins in incident CKD patients using a nationwide cohort of 3,562,882 US Veterans. The study aimed to determine whether TG-targeting therapies confer different kidney outcomes than statins in non-dialysis-dependent CKD, addressing prior evidence gaps and equivocal results. If TG-targeting agents show benefit (or lack thereof), the work can directly inform lipid-management choices to slow CKD progression.

Naim MAAZ, Thomas F, Streja E et al. · Clinical journal of the American Society of Nephrology : CJASN · (2026) · View on PubMed ↗

Is D-Dimer Associated With Disease Severity and Contralateral Slip Risk in Slipped Capital Femoral Epiphysis?

The study evaluated whether D-dimer levels in patients with slipped capital femoral epiphysis (SCFE) associate with disease severity and the risk of contralateral slip, and whether D-dimer improves existing prediction models. In a single-center retrospective cohort of 25 unilateral SCFE patients, D-dimer was analyzed alongside clinical factors (e.g., Loder stability, chronicity) and laboratory parameters to assess correlations with severity and future contralateral slipping. If validated, D-dimer could serve as an accessible biomarker to stratify SCFE risk and guide monitoring intensity.

Kurk MB, Albayrak K, Aydin A et al. · Journal of pediatric orthopedics · (2026) · View on PubMed ↗

Comparison of the 2025 ESC/EAS and 2026 ACC/AHA Guidelines for Dyslipidemia Management.

This study compared the 2025 ESC/EAS and 2026 ACC/AHA dyslipidemia management guidelines for prevention of atherosclerotic cardiovascular disease in clinical practice. Both guidelines emphasize that lowering LDL-C and other apolipoprotein B–containing lipoproteins earlier, deeper, and more durably reduces cardiovascular risk, but they differ in how prevention is operationalized through risk categorization and treatment targets. The comparison is clinically significant because it clarifies how guideline structure may change real-world statin/adjunct selection and LDL-C goal-setting for patients at different baseline risk levels.

Finocchiaro S, Mauro MS, Bordonaro C et al. · European journal of preventive cardiology · (2026) · View on PubMed ↗

Skin Impacts and Tradeoffs of GLP-1 Therapy: Improved Patient-Reported Outcomes of Inflammatory Skin Disease in the Era of “Ozempic Face”.

This survey-based study assessed patient-reported skin, hair, and nail changes associated with GLP-1 receptor agonist therapy in the context of “Ozempic Face,” focusing on inflammatory skin disease outcomes and tradeoffs relative to weight loss. It characterized the frequency and nature of dermatologic effects reported by patients using GLP-1RAs and linked these changes to weight management treatment. The clinical significance is that it provides patient-centered evidence to better counsel patients on expected skin-related benefits and risks during GLP-1 therapy.

Rao S, Midura I, Mangual KPS et al. · Dermatology and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Effects of creatine supplementation with and without exercise and diet intervention on body composition, cognitive function, and markers of health in middle-aged and older adults.

This randomized, double-blind, counterbalanced study in 73 healthy middle-aged and older adults (sedentary, with optional exercise-and-diet intervention) tested whether creatine monohydrate (CrM) supplementation (2×5 g/day) with or without exercise and diet changes body composition, cognitive function, and health markers. Participants were assigned to CrM versus maltodextrin placebo (PLA) and outcomes were measured across intervention groups, with specific results truncated in the abstract. If CrM improves body composition and cognition during lifestyle interventions, it could inform nutrition strategies for maintaining health and function in aging populations.

Chun J, Liu Y, Kibler GL et al. · Journal of the International Society of Sports Nutrition · (2026) · View on PubMed ↗ · Free PDF ↗



Generated automatically on August 13, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.