PubMed Trending Research Digest — September 16, 2026

Automated digest · 98 articles · 26 research areas · September 16, 2026

Overview

Across this week’s set of papers, a dominant theme is precision medicine built on biomarkers, stratification, and mechanistic targeting. Several oncology studies use modern molecular readouts—ctDNA-guided adaptive de-escalation in resected colon cancer, spatial/radiation-resistance signatures in glioblastoma, and proteogenomic/metabolic mechanisms in glioma and PDAC—to better time or tailor therapy and avoid overtreatment. In parallel, multiple immunotherapy-focused articles emphasize improving efficacy and durability (e.g., TIL therapy trajectories in melanoma, local IFNγ delivery to restore antigen presentation in medulloblastoma, and host immune regulators such as DUSP4 affecting CD8 function and CAR-T performance), while safety-focused work highlights the need for cardiac monitoring during immune checkpoint inhibitor therapy.

A second major theme is immune and inflammation as a cross-cutting driver of disease, spanning cardiovascular, renal, neurodegenerative, and infectious contexts. Reviews and mechanistic studies connect plaque/coagulation biology and post-MI immune remodeling to outcomes, while infection-related immune effects (latent CMV after MI; gut microbiota–inflammation links in post-stroke depression; and gut–brain serotonergic signaling in microbiota-driven hypertension) suggest new intervention points beyond traditional organ-centric models. In kidney disease, macrophage heterogeneity and cilia/cell-cycle control (e.g., TREM2+ niches in DKD; CDK6 inhibition and ciliary polycystin restoration in ADPKD) point toward niche-specific or pathway-specific therapies.

Finally, several papers advance translational infrastructure—computational pathology (a foundation model for intraoperative frozen sections), EHR-based maternal/infant outcome forecasting, and single-molecule/structural/epigenetic frameworks that make biology more measurable at scale. In neurodegeneration, multiple studies expand the molecular landscape of Alzheimer’s disease (microprotein atlases, co-pathology-informed target thinking, and genetics/medication exposome effects), while ALS-focused work continues to push therapeutic delivery and biomarker frameworks (EV-delivered ASOs, peripheral pTDP-43 systemic pathology, and base/ASO approaches). Together, these efforts reflect a broader shift toward integrating high-resolution measurement with targeted interventions and real-world implementation to improve outcomes.

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Targeted Oncology & Antibody-Drug Conjugates / Bispecifics

Oral KRAS G12D inhibitor GFH375 for previously treated advanced solid tumors with KRASG12D mutations: a phase 1 trial.

This phase 1 dose-escalation trial evaluated the oral KRAS G12D inhibitor GFH375 in patients with advanced solid tumors harboring KRASG12D mutations, assessing safety/tolerability, maximum tolerated dose, and pharmacokinetics. GFH375 was designed to bind both ON (GTP-bound) and OFF (GDP-bound) states of KRASG12D, with efficacy outcomes including objective response rate reported as secondary endpoints. If clinically active and tolerable, GFH375 would represent a mutation-specific therapeutic strategy for KRASG12D-driven cancers such as PDAC, CRC, and NSCLC.

Ai X, Song Z, Wu L et al. · Nature medicine · (2026) · 1 citations · View on PubMed ↗

Amivantamab plus pembrolizumab in previously untreated recurrent/metastatic head and neck squamous cell cancer: Results from the phase 1b/2 OrigAMI-4 study.

This phase 1b/2 OrigAMI-4 study cohort 2 evaluated first-line amivantamab (EGFR-MET bispecific antibody) plus pembrolizumab in previously untreated recurrent/metastatic head and neck squamous cell cancer (R/M HNSCC). The trial reported efficacy and safety outcomes for this combination in a population with poor prognosis, leveraging EGFR and MET overexpression and PD-L1–defined eligibility. If confirmed in larger studies, the regimen could provide a new targeted immunotherapy option for R/M HNSCC by combining EGFR/MET blockade with immune checkpoint inhibition.

Kao HF, Harrington K, Bhatia A et al. · Clinical cancer research : an official journal of the American Association for Cancer Research · (2026) · View on PubMed ↗

Perioperative Outcomes and Pathological Response After Neoadjuvant Nivolumab Plus Platinum Chemotherapy in Clinically Node-Negative Non-Small Cell Lung Cancer.

This pre-specified secondary analysis of the CReGYT-04 Neo-Venus registry studied perioperative outcomes and pathological response in 129 Japanese patients with clinically node-negative (cN0) stage IIA–IIIB non-small cell lung cancer (NSCLC) treated with neoadjuvant nivolumab plus platinum-doublet chemotherapy. Compared across clinical nodal status groups (cN0 vs cN1–2), the study found that neoadjuvant nivolumab-based chemoimmunotherapy was associated with acceptable perioperative outcomes and measurable pathological responses in the cN0 population. These findings support the feasibility of neoadjuvant nivolumab plus platinum chemotherapy in cN0 NSCLC and help refine expectations for surgical and tumor-downstaging outcomes in this subgroup.

Watanabe T, Nomura K, Takamori S et al. · Annals of surgical oncology · (2026) · View on PubMed ↗

Tambotatug Pelitecan in Small-Cell Lung Cancer after Platinum-Based Therapy.

This phase 3, multicenter, open-label randomized trial studied tambotatug pelitecan (Tam-Peli), an antibody-drug conjugate targeting B7-H3, versus topotecan in patients with small-cell lung cancer (SCLC) that progressed after first-line platinum-based therapy. The key finding was that tambotatug pelitecan improved overall survival compared with topotecan, with corresponding benefits in progression-free survival and objective response as assessed by investigators. The trial supports B7-H3–directed antibody-drug conjugate therapy as a new treatment option for relapsed extensive-stage SCLC after platinum failure.

Zhao Y, Liu H, Meng X et al. · The New England journal of medicine · (2026) · View on PubMed ↗

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Other Biomedical Cell Biology & Cellular Stress Pathways (ferroptosis/cuproptosis/cilia assembly/glycogen QC/etc.)

Cysteine excess triggers a mitochondrial iron-dependent cell death.

This study used a genome-wide CRISPR screen to determine how excess cysteine triggers mitochondrial iron-dependent cell death (ferroptosis-like death) in cells. The authors identified mitochondrial iron transporters as essential mediators, showing that limiting mitochondrial iron suppresses cysteine-induced death and preserves iron-sulfur cluster proteins and respiration. These findings link cysteine toxicity to mitochondrial iron handling and suggest that targeting mitochondrial iron transport could modulate cysteine-driven ferroptotic cell death.

Nakamura T, Inoki A, Das NK et al. · Nature metabolism · (2026) · 1 citations · View on PubMed ↗

Quality control of glycogen through direct ubiquitylation by RNF213.

This work investigated how cells quality-control aberrant glycogen and prevent polyglucosan buildup, focusing on the E3 ubiquitin ligase RNF213 and autophagy of ubiquitylated glycogen. The authors found that RNF213-dependent ubiquitylation licenses autophagy of aberrant glycogen, and mice with loss of RNF213 ligase activity accumulated polyglucosan in brain regions including cerebellum, pons, and hippocampus. The study identifies a specific ubiquitin–autophagy pathway for glycogen quality control with direct relevance to polyglucosan body diseases affecting the brain.

Yip MCJ, Naydenova K, Otten EG et al. · Nature · (2026) · View on PubMed ↗

ACTA2-directed actin filaments license STING trafficking and activation for antiviral immunity and autoimmune pathogenesis.

This study investigated how the STING pathway is activated through intracellular trafficking, identifying an actin-based transport mechanism licensed by the smooth muscle actin isoform ACTA2. Using superresolution live imaging and in vitro reconstitution, the authors showed that STING becomes punctate and activated while moving along ACTA2 filaments, and that this ACTA2-directed network is required for antiviral interferon responses against HSV-1 while also driving pathological interferon production. The work is significant because it links a specific cytoskeletal regulator (ACTA2) to STING trafficking and activation, with implications for both antiviral immunity and autoimmune pathogenesis.

Hou X, Wu Q, Du Y et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

FAP53 facilitates formation of microtubule doublets.

This study identified FAP53 as a molecular factor that facilitates formation of microtubule doublets (MTDs), a key step in cilia biogenesis. In vitro reconstitution showed recombinant FAP53 enhances B-tubule assembly in the presence of preassembled microtubule scaffolds but cannot initiate de novo assembly from free tubulin, and in HeLa cells coexpression of CFAP53 with CFAP20 induced ectopic MTD-like structures. The findings are significant because they clarify how B-tubule nucleation is scaffold-dependent and provide a mechanistic entry point for understanding cilia assembly defects.

Li M, Chen G, Chen Z et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Encoded and non-genetic protein variants expand human functional proteome.

This proteogenomics study used a large-scale dataset from 29 healthy human tissues to identify and functionally evaluate encoded (genetically specified) and non-genetic protein variants coexisting within the human functional proteome. It localized 13,910 confidently localized variants corresponding to 7,215 unique single amino acid substitutions and quantified their abundance alongside reference proteoforms. The significance is a more complete map of human proteome diversity, enabling better interpretation of how variants arise and how they may affect protein function and disease susceptibility.

Tretyachenko V, Leiman T, Morgenstern D et al. · Nature · (2026) · View on PubMed ↗

Myeloid cell replacement induces intercellular mitochondrial transfer and restores metabolism in a mouse model of mitochondrial disease.

The study tested whether myeloid cell replacement in a mouse model of mitochondrial disease (Friedreich’s ataxia due to frataxin deficiency) can restore metabolism and improve organ function. Myeloid replacement promoted intercellular mitochondrial transfer from microglia and macrophages to CNS cells and cardiomyocytes, increasing oxidative phosphorylation and ATP synthesis gene expression and improving survival and growth. Scientifically and therapeutically, the results support mitochondrial transfer as a disease-modifying strategy for frataxin-related mitochondrial dysfunction.

Cho H, Sayana R, Koladiya A et al. · Nature communications · (2026) · View on PubMed ↗

Odorant receptor coexpression and multi-expression in the dengue mosquito.

The study sequenced transcriptomes of 46,000 female Aedes aegypti antennal neurons to map odorant receptor (OR) expression patterns and determine the extent of OR coexpression. It found that about half of neuronal subtypes coexpress multiple receptors, but coexpression occurred almost exclusively among receptors from the same OR family rather than across families. This refines models of insect olfaction beyond a strict one-receptor-per-neuron rule and improves understanding of how mosquito chemosensory coding may be organized.

David E, Dos Anjos VL, Kotb SM et al. · Nature communications · (2026) · View on PubMed ↗

Hepassocin prevents age-related liver senescence and facilitates liver regeneration by activating AMPK.

The study examined whether the hepatokine Hepassocin (HPS) prevents age-related liver senescence and supports liver regeneration by activating AMPK, using aged mice and elderly human samples. It found decreased circulating and intrahepatic HPS in aged mice and elderly humans, blunted HPS upregulation after two-thirds partial hepatectomy in aged mice, and (from the truncated abstract) evidence that HPS promotes regeneration and reduces senescence via AMPK activation. These findings suggest HPS–AMPK signaling as a potential therapeutic axis to counteract impaired regenerative capacity during liver aging.

Yang Y, Chen H, Xiang S et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗

Efficient experimental characterization of the GPCRome via deep receptor scanning.

The study developed a “deep receptor scanning” platform to experimentally characterize 766 human GPCRs and 174 splice variants in parallel, assessing transcript abundance, translational efficiency, and plasma-membrane expression. It enabled quantitative, high-throughput profiling of canonical versus alternative GPCR transcripts and their surface expression in a recombinan[t] experimental context. This provides a scalable functional map of the understudied human GPCRome that can accelerate target selection and drug discovery.

Tedman A, Goel M, Shah S et al. · Nature communications · (2026) · View on PubMed ↗

Copper ion-induced MYH9 polymerization executes cuproptosis.

The study investigated the execution mechanism of cuproptosis in cells by identifying copper-dependent proteins and testing how intracellular copper handling triggers cell death. Copper binding induced polymerization of myosin heavy-chain 9 (MYH9), disrupting the actin cytoskeleton and causing cuproptotic cell death, while the compound HThPA induced cuproptosis via Nur77 binding that depleted glutathione (GSH) and released free copper from intracellular stores. These findings define MYH9 polymerization as a cuproptosis execution step and implicate Nur77–GSH–copper mobilization as a druggable pathway.

Wu LZ, Mi XY, Liu ZJ et al. · Cell · (2026) · View on PubMed ↗

Structural underpinnings of human Slo1 inhibition by scorpion and fungal toxins.

This structural pharmacology study used single-particle cryo-EM, liposome flux assays, and toxin-binding assays to define how small molecules inhibit human Slo1 (hSlo1) potassium channels, comparing scorpion toxins with fungal mycotoxins. The key finding is that indole diterpene fungal mycotoxins (paxilline and penitrem A) bind deep in a pocket within the putatively closed hSlo1 pore, sterically restricting channel opening and slowing dissociation of a fluorescent charybdotoxin derivative. Scientifically, the work provides a mechanistic blueprint for designing Slo1 inhibitors that act via pore-pocket gating blockade rather than classical permeation-blocker mechanisms.

Kallure GS, Pal K, Prather GW et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Diaphragmatic Breathing as an Adjunctive Approach in Gastroesophageal Reflux Disease: Narrative Review of Its Mechanistic Basis and Clinical Evidence.

This narrative review examined diaphragmatic breathing (DB) as an adjunct non-pharmacologic intervention for gastroesophageal reflux disease (GERD), focusing on mechanistic links to anti-reflux barrier function via crural diaphragm activity. It reports that DB may improve reflux-related symptoms in patients who do not fully respond to proton pump inhibitors by strengthening the physiological barrier against reflux. The clinical significance is that DB could offer a low-risk adjunct strategy for GERD management, especially for PPI-refractory patients.

Semwal A, Jha S, Kumar A et al. · Advances in mind-body medicine · (2026) · View on PubMed ↗

Intravenous Immunoglobulin Add-On in Newly Diagnosed Idiopathic Inflammatory Myopathies: A Randomized Clinical Trial.

This randomized clinical trial studied whether adding three cycles of intravenous immunoglobulin (IVIG) improves outcomes in adult patients with newly diagnosed idiopathic inflammatory myopathies (IIM) treated with high-dose prednisone (1 mg/kg/day, max 80 mg/day). The key finding was that add-on IVIG was tested against placebo with the primary endpoint at week 12 to determine superior improvement with acceptable safety. If effective, this would support IVIG as an evidence-based escalation strategy for newly diagnosed IIM beyond corticosteroids.

Özkaynar P, Evers S, Kamperman R et al. · JAMA neurology · (2026) · View on PubMed ↗

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Public Health & Global Burden of Disease

Burden of cancer in Africa, 1990-2023: a systematic analysis from the Global Burden of Disease Study 2023.

This systematic analysis used the Global Burden of Disease Study 2023 to estimate fatal and non-fatal cancer burden across 54 African countries from 1990–2023 for 48 cancer types. The key finding was a disproportionately rising cancer burden across Africa despite major gaps in cancer surveillance data, providing age- and sex-disaggregated estimates to quantify trends. These results are significant for informing regional cancer control policies and for monitoring progress toward global health targets.

The Lancet. Oncology · (2026) · View on PubMed ↗ · Free PDF ↗

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Solid Tumor Mechanisms, Resistance & Translational Biomarkers

Gliomas phenocopy an inborn error of metabolism to drive neuronal activity and tumor growth.

This study combined human brain tissue metabolomics with mechanistic experiments to show how high-grade gliomas phenocopy an inborn error of metabolism via guanidinoacetate (GAA) dysregulation. Glioma cells accumulated and secreted GAA due to imbalanced creatine synthesis pathway enzyme activities, and GAA increased neuronal excitability in a manner linked to GAMT (GAA N-methyltransferase) deficiency, thereby promoting neuron–glioma interactions that drive tumor growth. The work is significant because it connects a specific metabolic intermediate (GAA) to neuronal activity and glioma progression, suggesting metabolic targeting as a potential therapeutic angle.

Abdullah KG, Miki K, Edgar CK et al. · Cell · (2026) · View on PubMed ↗ · Free PDF ↗

The Spatiotemporal Evolution of Radiation Resistance in Glioblastoma.

This study analyzed the spatiotemporal evolution of radiation resistance in glioblastoma (GBM) using a radio-resistance signature score (RRSS) derived from glioma sphere-forming cells (GSCs) that recapitulate GBM transcriptomic states. RRSS could assess radiation response in both glioma cell lines and GBM patients, and both transdifferentiated and irradiated glioma cells showed increased radiation resistance. Scientifically, it provides a framework for mapping when and where resistance emerges during GBM progression and treatment, which could inform timing and targeting of radiosensitizing strategies.

Wu L, Cheng L, Huang B et al. · Neuro-oncology · (2026) · View on PubMed ↗

DHODH inhibition drives albumin-mediated drug resistance through TERF2IP lactylation-activated macropinosome-mitochondria contact.

The study examined how dihydroorotate dehydrogenase (DHODH) inhibition affects macropinocytosis and chemoresistance in cancer cells, using CRISPR-Cas9 and small-molecule screening and focusing on TERF2IP. DHODH inhibition drove metabolic reprogramming toward glycolysis and lactate accumulation, which activated lysine 208 lactylation of TERF2IP and promoted epiregulin transcription that activated EGFR signaling. These findings link pyrimidine-synthesis blockade to lactylation-dependent transcriptional control of EGFR-mediated resistance, suggesting a mechanistic vulnerability to target in DHODH-driven tumor therapy.

Yuan J, Wang T, Ma Y et al. · Nature communications · (2026) · View on PubMed ↗

Spatial analysis reveals the evolving organization of IDH-mutant glioma.

This study used spatial transcriptomics and spatial proteomics to map the evolving organization of IDH-mutant gliomas across histological grades in adult tumors. It identified a functional white–gray matter junction that restricts cortical invasion and is associated with shifts in tumor composition and phenotypes, with oligodendrocyte progenitor (OPC)-like malignant cells preferentially traversing this junction. These spatial organization principles provide actionable targets for understanding and potentially intercepting IDH-mutant glioma expansion.

Hoefflin R, Greenwald AC, Galili Darnell N et al. · Cancer cell · (2026) · View on PubMed ↗

Pancreatic ductal adenocarcinoma: The Vision of Heracles.

This perspective article reviews why pancreatic ductal adenocarcinoma (PDAC) resistance is not solely KRAS-driven and highlights overlooked contributors including PanIN/IPMN biology, peripancreatic fat, stromal mechanics, myeloid–neural circuits, metabolic rewiring, and systemic host responses. It proposes precision interception using spatial-functional proteogenomic classification and the “Heracles Protocol” (measure, prime, strike, and adapt), integrating approaches such as AI pathology, exosomal delivery, and CRISPR-based strategies. The framework aims to guide more adaptive, multi-compartment therapeutic development for PDAC.

Mota Reyes C, Goetz MR, Algül H et al. · Cancer cell · (2026) · View on PubMed ↗

P-Loop/αC-Helix Compressing Mutations and Exon 20 Insertions in EGFR-Mutant NSCLC: A Rapidly Evolving Therapeutic Landscape.

This narrative review examined the structure-function classification of EGFR P-loop/αC-helix compressing (PACC) mutations and exon 20 insertions (ex20ins) and summarized how these distinct kinase-domain alterations affect sensitivity to EGFR tyrosine kinase inhibitors (TKIs) and subsequent treatment strategies in EGFR-mutant non-small cell lung cancer. The key finding is that PACC and ex20ins tumors generally show reduced sensitivity to currently approved EGFR TKIs for classical sensitizing mutations and are often treated with chemotherapy, while emerging therapies and resistance mechanisms are rapidly evolving. Clinically, the review underscores the need for mutation-specific therapeutic selection and ongoing trial enrollment for these EGFR subsets.

Monaca F, Randulfe I, Heymach JV et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗

SelO functions as a tumor suppressor through AMPylating Cdk5rap3.

This mechanistic cancer study investigated the tumor-suppressive role of SELENOO (SelO) and its AMPylation target in mammalian cells and mice, focusing on how SelO modifies CDK5 regulatory subunit-associated protein 3 (Cdk5rap3). The authors found that SelO is induced by chemotherapy, that SelO knockout in mice promotes primary tumor development and metastasis, and that SelO AMPylates Cdk5rap3 at T328 to enhance ARF interaction and suppress proliferation and migration. These results identify SelO–Cdk5rap3 AMPylation as a potential therapeutic vulnerability and biomarker axis in cancer.

Wu L, Wu J, Xie W et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

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Infectious Disease Mechanisms & Antiviral/Vaccine Strategies

Programmed ribosomal frameshifting triggers translational stress to promote viral replication.

This study examined how programmed ribosomal frameshifting (PRF) in SARS-CoV-2 activates host translational stress pathways to support viral replication. A minimal SARS-CoV-2 PRF element activated the GCN2 arm of the integrated stress response independently of the canonical sensor ZAKα, shutting off host translation early in infection and being required for viral propagation in cells and human airway organoids. By identifying DRG1 and IGF2BP3 as key mediators, the findings highlight specific host factors and stress-response wiring that could be targeted to limit viral replication.

Xavier A, Kolling M, Bourke AM et al. · Cell · (2026) · View on PubMed ↗ · Free PDF ↗

A Genetically Encoded Marker for Imaging of Internal Plasmodium Membranes.

This 2026 study investigated a genetically encoded fluorescence marker to image internal Plasmodium membranes in malaria parasites. It found that the commonly used membrane dye BODIPY TR Ceramide adversely affects Plasmodium cell viability during live-cell imaging, motivating development of IMMP (Internal Membrane Marker for Plasmo) as a broadly marking internal membrane alternative. Scientifically, IMMP enables safer, longer-term live-cell fluorescence microscopy of internal membrane dynamics in Plasmodium.

Zink L, Reuschenbach V, Ahmed SS et al. · Molecular microbiology · (2026) · View on PubMed ↗

Occult hepatitis B virus infection.

This review studied occult hepatitis B virus (HBV) infection (OBI), defined as replication-competent HBV DNA in liver or blood in individuals seronegative for hepatitis B surface antigen. It reports that OBI prevalence varies widely by exposure/endemicity and that diagnosis is difficult because HBV DNA levels are extremely low and fluctuate over time, with serology (e.g., anti-HBc) being insufficient alone. The clinical significance is that it clarifies why OBI requires careful diagnostic strategies and informs screening considerations for at-risk populations.

Mak LY, Hui RW, Pollicino T et al. · Nature reviews. Gastroenterology & hepatology · (2026) · View on PubMed ↗

Redox cycling of viral RNA polymerase controls picornavirus replication.

The study used porcine genome-wide CRISPR/Cas9 screens to identify host factors controlling picornavirus replication and focused on methionine sulfoxide reductase B3 (MSRB3) for foot-and-mouth disease virus (FMDV). MSRB3 was essential for FMDV replication because it eliminates methionine oxidation of the viral 3D polymerase, stabilizing its expression, and the work implicated RSAD1 as a catalyst of methionine oxidation of the FMDV 3D polymerase. This mechanistic redox-control pathway reveals a host-dependent vulnerability that could be targeted to suppress picornavirus replication.

Li WW, Zhu ZY, Zhang W et al. · Nature communications · (2026) · View on PubMed ↗

Acyl carrier protein is essential for apicoplast biogenesis in malaria parasites independent of fatty acid synthesis.

This eLife study examined the role of acyl carrier protein (ACP) in Plasmodium malaria parasites, testing whether ACP is required for apicoplast biogenesis independent of type II fatty acid synthesis (FASII). Using ACP knockout or ligand-dependent knockdown approaches, it found that ACP is essential for apicoplast biogenesis even when fatty acid synthesis is not the critical driver of fitness in the tested context. The scientific significance is that ACP represents a potential malaria vulnerability distinct from canonical FASII targets, informing new antimalarial strategies.

Geher SWR, Falekun S, Pita-Aquino JN et al. · eLife · (2026) · View on PubMed ↗

Respiratory Syncytial Virus-Related Hospitalizations Among Infants Receiving Nirsevimab.

This test-negative case-control study evaluated clinical effectiveness of nirsevimab, a long-acting monoclonal antibody, in preventing RSV-related emergency department visits, hospitalizations, and ICU admissions among infants in Ontario and Quebec, Canada. The key finding was an estimate of nirsevimab’s real-world effectiveness using data from seven tertiary pediatric hospitals after public funding began in fall 2024. This is clinically significant because it quantifies how well nirsevimab prevents severe RSV outcomes in routine practice.

Buchan SA, Xie J, Bhatt M et al. · JAMA network open · (2026) · View on PubMed ↗

DNA polymerase I is required for the Hachiman-family anti-phage defense system.

This study investigated how DNA polymerase I (PolA; gene polA) contributes to the Hachiman-family abortive infection (Abi) anti-phage defense system in Escherichia coli, focusing on the HamA/HamB nuclease–helicase effector complex and the AbpAB variant. Using a temperature-sensitive polA mutant (polA12), the authors found that PolA is required for AbpAB- and HamAB-mediated phage restriction, while RNase HI prevents AbpAB-dependent growth inhibition during uninfected growth. Scientifically, the work links Abi effector function to host DNA replication/repair machinery, identifying PolA as a critical host factor for Hachiman-family phage defense.

Takita S, Moroi R, Terasaki H et al. · Journal of bacteriology · (2026) · View on PubMed ↗ · Free PDF ↗

The mRNA-Based Therapeutic Vaccine NTX250 Induces Potent Antitumor Immunity in HPV-Driven Cancers.

This preclinical study developed the mRNA-based therapeutic vaccine NTX250 and evaluated its ability to induce antitumor immunity in HPV-driven cancers. The key finding was that NTX250 elicited potent, tumor-targeted immune responses that translated into strong antitumor activity in HPV-associated settings. Clinically, NTX250 represents a therapeutic vaccination strategy aimed at eliminating persistent HPV infection and improving outcomes in HPV-driven malignancies beyond prophylactic HPV vaccines.

Leong M, Liu W, Fay N et al. · Cancer research · (2026) · View on PubMed ↗

CRISPR and yeast two-hybrid screens identify CD81 as a proviral host factor for PRRSV.

This study used CRISPR screening (targeting genes encoding cell-surface CD proteins) combined with yeast two-hybrid screening to identify host factors required for porcine reproductive and respiratory syndrome virus (PRRSV) infection, focusing on CD81. The authors found that the tetraspanin CD81 is a proviral host factor that directly interacts with PRRSV glycoprotein 5 (GP5), and that CD81 knockdown reduced PRRSV infection while CD81 overexpression increased it; antibody blockade of CD81 restricted infection in Marc-145 cells and primary porcine alveolar macrophages. These results identify CD81–GP5 interaction as a mechanistic vulnerability that could be exploited for antiviral interventions against PRRSV.

Chen Y, He Z, Pan Y et al. · Journal of virology · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Immunotherapy & Cellular Therapies (TIL, CAR-T, T-cell Engagers, Checkpoint Safety)

Single-cell tracking reveals tumor-reactive T cell plasticity during melanoma TIL therapy.

This study used longitudinal single-cell RNA sequencing and T-cell receptor sequencing to track tumor-reactive T cell plasticity during adoptive TIL therapy in seven metastatic melanoma patients. Tumor-reactive CD8+ T cells were reinvigorated from exhaustion and adopted HLA-II-high or KLF2-high transcriptional profiles across time points spanning baseline tumors, ex vivo expansion, and post-infusion blood and tumor biopsies. The results are significant because they define clonal/transcriptional trajectories of therapeutic T cells, informing strategies to improve durability and function of TIL-based therapies.

Sandholzer MT, Serger C, Liner AG et al. · Cell reports. Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Avoidance of cardiac toxicity during the application of immune checkpoint inhibitors: a safety systematic review combining network meta-analysis and pharmacovigilance study.

This 2026 safety-focused study investigated cardiac toxicity risk from immune checkpoint inhibitor (ICI) therapy by combining a systematic review with network meta-analysis and pharmacovigilance analysis of the FAERS database. It aimed to quantify overall cardiac toxicity incidence, identify common cardiac toxicity types, and determine which specific ICIs require the most cardiac monitoring. The findings are intended to improve clinical safety surveillance strategies for patients receiving ICIs.

Chen H, Shan Y, Xu H et al. · Frontiers in immunology · (2026) · View on PubMed ↗

Targeting CD38 with bispecific antibody XmAb 18968 in patients with relapsed/refractory acute myeloid leukemia and T-cell acute lymphoblastic leukemia.

The phase 1 multicenter clinical trial evaluated XmAb18968, a CD38-CD3 bispecific T-cell engager with an Fc modification to reduce non-selective effector activation, in adults with relapsed/refractory acute myeloid leukemia (AML) and T-cell acute lymphoblastic leukemia (T-ALL). The study enrolled 22 patients (13 AML, 9 T-ALL) and assessed safety and clinical outcomes, with reported grade ≥3 adverse events (details truncated in the abstract). Clinically, targeting CD38 with XmAb18968 offers a potential immunotherapy option for RR AML and T-ALL, and the trial informs dosing and tolerability for further development.

Guru Murthy GS, Shah B, Badar T et al. · Leukemia · (2026) · View on PubMed ↗

DUSP4 promotes anti-tumor CD8+ T cell function and boosts CAR-T cell efficacy in mouse colorectal cancer.

The study investigated how the dual-specificity phosphatase DUSP4 regulates anti-tumor CD8+ T cell function and CAR-T efficacy, using human colorectal cancer (CRC) expression correlations and an AOM/DSS-induced mouse CRC model. DUSP4 deficiency promoted tumorigenesis and impaired CD8+ T cell-mediated anti-tumor immunity, while lower DUSP4 expression in CRC patients associated with shorter survival. These results identify DUSP4 as a regulator that could be leveraged to enhance CAR-T performance in solid tumors like CRC.

Li H, Koh CKT, Zhang T et al. · Nature communications · (2026) · View on PubMed ↗

Local delivery of interferon restores antigen presentation and sensitizes medulloblastoma to T cell killing.

This preclinical study used a syngeneic mouse model of medulloblastoma to test whether local interferon delivery can restore antigen presentation and sensitize tumors to T cell killing. The authors found that tumor control depended on T cell-derived IFNγ, which induces MHC class I on tumor cells, and that delivering IFNγ directly into tumors via convection restored antigen presentation and improved susceptibility to CD8+ T cell-mediated killing. The work supports local IFNγ delivery as a strategy to convert immunologically cold medulloblastoma into a more immunogenic, T cell–responsive state.

Eisemann T, Chambers KR, Beigi Masihi M et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Top advances of the year in autologous cellular therapy in melanoma and solid tumors.

This narrative review summarized major advances in autologous cellular therapy for melanoma and solid tumors, emphasizing therapies such as lifileucel (tumor-infiltrating lymphocytes, TIL) and emerging antigen-targeted T-cell receptor (TCR) approaches including PRAME-targeted TCR T cells. The key finding was that lifileucel showed durable efficacy in the C-144-01 trial with an ORR of 31.4% in a heavily pretreated population, with real-world data supporting effectiveness. Scientifically and clinically, the review highlights how improved durability and antigen-specific engineering are expanding the role of autologous cellular therapies across solid tumors.

Loo K, Betof AS · Cancer · (2026) · View on PubMed ↗

Engineered Bacteriophages in Cancer Immunotherapy: Emerging Concepts and Potential Integration with CAR-T Cell Therapy.

This review article synthesized emerging concepts for engineered bacteriophages in cancer immunotherapy and discussed how they might integrate with CAR-T cell therapy. The key finding is that engineered phages can be modularly designed to deliver tumor-associated antigens and therapeutic payloads (e.g., cytokines/chemokines or suicide genes) while overcoming barriers such as antigen heterogeneity and immunosuppressive tumor microenvironments. Scientifically and clinically, it frames engineered phage platforms as potential adjuncts to CAR-T by improving antigen presentation, trafficking, and intratumoral immune activation.

Alrahimi J · Folia biologica · (2026) · View on PubMed ↗ · Free PDF ↗

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Neurodegeneration (Alzheimer’s/ALS/Huntington’s) Biomarkers, Pathology & Therapeutics

Peripheral TDP-43 pathology in amyotrophic lateral sclerosis: toward a systemic proteinopathy.

This article reviewed and synthesized evidence that ALS is accompanied by peripheral (non-neural) pathology characterized by phosphorylated TDP-43 (pTDP-43) accumulation beyond the brain, spinal cord, and motor nerves. The key finding is that pTDP-43 pathology has been reported in multiple peripheral tissues—including skeletal and cardiac muscle, skin, minor salivary glands, gastrointestinal tract, and lymph nodes—supporting a systemic proteinopathy model. This is significant because it reframes ALS as potentially involving whole-body spread or multi-tissue involvement, which could influence biomarker development and therapeutic targeting.

Codron P, Miranda M, Garnier M et al. · Acta neuropathologica · (2026) · View on PubMed ↗

Neural Stem Cell-Derived Extracellular Vesicles Improve CNS Delivery and Therapeutic Efficacy of Antisense Oligonucleotide in Amyotrophic Lateral Sclerosis.

This preclinical study developed neural stem cell-derived extracellular vesicles (NSC-EVs) as carriers for antisense oligonucleotides (ASOs) to improve central nervous system delivery and therapeutic efficacy in amyotrophic lateral sclerosis (ALS). Passive loading produced NSC-EV-ASO complexes that showed markedly enhanced neuronal uptake in vitro and improved CNS delivery/efficacy compared with free ASOs. The approach is significant because it targets key ASO limitations—poor CNS penetration, inefficient uptake, and rapid clearance—potentially improving ASO-based ALS treatment feasibility.

Zheng Y, Ellison TJ, Garrard R et al. · Journal of extracellular vesicles · (2026) · View on PubMed ↗

Immune dysregulation and stem-like CD8+ T cell enrichment in type 1 diabetes pancreatic lymph nodes.

This 2026 human study analyzed immune dysregulation in type 1 diabetes by profiling pancreatic lymph nodes using mass cytometry, single-cell RNA sequencing (scRNA-seq), and T-cell receptor (TCR) profiling. It found enrichment of CD8+ T stem cell memory-like (TSCM-like) cells and an inflammatory cytokine gene signature (including IFITM3 and LTB) with altered terminal differentiation regulators (BCL6, BCL3) in T1D pancreatic lymph nodes. These findings suggest a stem-like CD8+ T cell–skewed, inflammation-associated immune state in the pancreatic lymph node niche that may help explain T1D pathogenesis and guide targeted immunotherapies.

Peters LD, Seay HR, Smith JA et al. · The Journal of clinical investigation · (2026) · View on PubMed ↗

UA-30 ameliorates motor deficits through RalA-mediated mitophagy in ALS mice.

This 2026 preclinical study tested the small-molecule inhibitor UA-30, which targets RalA, for therapeutic effects in an ALS mouse model (SOD1G93A). It found that oral UA-30 given for 6 weeks after onset of motor deficits extended lifespan and improved motor function, with UA-30 ameliorating deficits via RalA-mediated mitophagy. The results support RalA/mitophagy as a mechanistic therapeutic axis for ALS and provide proof-of-concept for UA-30–based intervention.

Zhang B, He Y, Su T et al. · The Journal of clinical investigation · (2026) · View on PubMed ↗

Alzheimer’s disease heterogeneity and co-pathologies: Defining novel targets, biomarkers, modalities, and research methodologies.

This 2026 article studied Alzheimer’s disease (AD) heterogeneity and co-pathologies to define novel targets, biomarkers, modalities, and research methodologies. It found that multiple co-pathologies (e.g., cerebral amyloid angiopathy, Lewy body pathology, α-synuclein, and TDP-43/lpTDP-43 encephalopathy) and diverse biological processes (vascular, proteinopathic, metabolic, immune) jointly shape clinical expression and therapeutic response, with advances in biomarkers such as seed amplification assays, proteomic signatures, and emerging PET tracers. Scientifically, it frames AD as a multi-mechanism condition to guide more precise biomarker stratification and target discovery.

Tansey MG, Bozeat S, Ackerman P et al. · Alzheimer’s & dementia (New York, N. Y.) · (2026) · View on PubMed ↗

Anti-Amyloid Antibodies in the Treatment of Alzheimer’s Disease: An Umbrella Review.

This umbrella review evaluated FDA- and EMA-approved anti-amyloid antibodies—lecanemab and donanemab—in people with Alzheimer’s disease using systematic reviews/meta-analyses. Across included evidence, the key findings were that these monoclonal antibodies reduce brain beta-amyloid (including PET measures) while carrying characteristic safety risks that must be weighed against cognitive/imaging benefits. Clinically, consolidating efficacy and adverse-event profiles for lecanemab and donanemab helps clinicians and patients make more informed treatment decisions in AD.

Kalampokini S, Keramidiotis I, Frontistis A et al. · Journal of clinical medicine · (2026) · View on PubMed ↗

A microprotein atlas of the human frontal cortex in Alzheimer’s disease.

This study investigated microproteins (≤150 amino acids) in the human frontal cortex in Alzheimer’s disease by integrating transcriptomics, mass spectrometry, and deep-learning-predicted spectra across 600+ postmortem samples. It identified 1,067 microproteins with high-confidence spectral support that were absent from reviewed UniProtKB entries, and found a subset differentially expressed in AD. The scientific significance is that it expands the Alzheimer’s disease molecular landscape by providing a curated microprotein atlas that can enable new biomarker and therapeutic target discovery.

Miller B, Vieira de Souza E, Lau C et al. · Nature aging · (2026) · View on PubMed ↗

All of Us diversity and scale yield context-dependent improvements in polygenic prediction.

The study used 245,388 whole-genome sequences from the All of Us (AoU) program combined with UK Biobank data to develop and evaluate multiancestry polygenic risk scores (PRSs) for 32 traits and diseases across ancestrally diverse participants. Increased genetic and health diversity in AoU improved PRS accuracy for several traits, particularly in under-represented populations, while performance depended on ancestry, methodology, and genetic architecture. These findings support scaling diverse genomic cohorts to reduce health disparities in PRS-based risk prediction.

Tsuo K, Shi Z, Ge T et al. · Nature genetics · (2026) · View on PubMed ↗

Loss of interruption in the HTT CAG repeat is associated with somatic expansion and loss of medium spiny neurons in Huntington’s disease.

This study examined how loss of interruption (LOI) in the HTT CAG repeat relates to somatic CAG expansion and medium spiny neuron (MSN) loss in Huntington’s disease patients. MSNs with large (111–150 CAG) and very large (>150 CAG) somatic expansions were rare early but increased with disease duration, and the deleterious CAG-CCG LOI modifier increased the proportion of MSNs with large/very large expansions by ~5-fold. The results strengthen the causal link between somatic expansion dynamics and MSN degeneration, supporting LOI status as a prognostic modifier in HD.

Kay C, Levesley J, Mätlik K et al. · Neuron · (2026) · View on PubMed ↗

N-of-1 investigational study of a novel antisense oligonucleotide drug in CHCHD10-related ALS shows early signs of efficacy.

This n-of-1 open-label investigational study evaluated the antisense oligonucleotide drug nL-CHCHD-001 in one participant with CHCHD10-related ALS carrying the p.Arg15Leu variant. The trial screened 320-gapmer ASOs, selected a lead candidate for specificity and non-clinical safety, and delivered six intrathecal doses over 12 months (three 50 mg then three 75 mg) to assess 12-month changes in functional, cognitive, quality-of-life, respiratory, and neurofilament outcomes. Early signals of efficacy support further development of non-allele-selective CHCHD10 knockdown ASO therapy for this rare dominantly inherited ALS subtype.

Cousin MA, Dagli AI, Mignon L et al. · Med (New York, N.Y.) · (2026) · View on PubMed ↗

Cardiometabolic medication exposures and cognitive outcomes in Alzheimer’s disease.

This study analyzed whether exposure to seven classes of cardiometabolic medications is associated with cognitive trajectories in Alzheimer’s disease using linear mixed-effects models with time-varying exposure in three cohorts (National Alzheimer’s Coordinating Center, n=28,044; Australian Imaging, Biomarkers and Lifestyle, n=1,708; Health and Aging Brain Study, n=1,425). Cardiometabolic medication classes showed distinct associations with longitudinal cognitive outcomes measured by CDR-SB, including differences by subgroup factors such as APOE ε4 status and baseline age group. The results suggest that the “medication exposome” may meaningfully shape cognitive decline in Alzheimer’s disease and could inform medication management and risk stratification.

Wang Y, Goudey B, Masters CL et al. · Age and ageing · (2026) · View on PubMed ↗

Clinical management of clonal hematopoiesis.

This Cancer review summarized clinical management considerations for clonal hematopoiesis, including clonal hematopoiesis of indeterminate potential (CHIP) and clonal cytopenia of undetermined significance (CCUS). It emphasizes that specific somatic mutations and clonal features in peripheral blood increase risk of progression to myelodysplastic syndromes and acute myeloid leukemia, while also contributing to systemic effects beyond malignancy. The clinical significance is that it guides risk stratification and monitoring strategies for an increasingly detected age-related premalignant condition.

Chien KS, Garcia-Manero G · Cancer · (2026) · View on PubMed ↗

Astrocytes in Neurodegeneration: Spatial States, Crosstalk, and Emerging Therapies.

This review studied astrocytes in neurodegeneration by integrating single-cell and spatial transcriptomic evidence across Alzheimer’s disease, Parkinson’s disease, ALS, Huntington’s disease, and rare primary astrocytopathies. The key finding was that astrocytes adopt heterogeneous, regionally patterned spatial states that align with neuronal vulnerability and converge on four mechanistic dysfunction axes: glutamate homeostasis breakdown, impaired ion/water buffering, lysosomal/autophagic insufficiency, and maladaptive inflammatory-stress signaling. Scientifically, it supports emerging spatial multi-omics and therapy development strategies targeting these convergent astrocyte dysfunction pathways.

Steger L, Rothhammer V, Zunke F · Molecular neurobiology · (2026) · View on PubMed ↗

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Neurodevelopmental & Neuropsychiatric Epidemiology/Consensus

Evidence-based atlas of risk and protective factors for psychotic disorders: an umbrella review to inform personalized prognosis and prevention.

This umbrella review synthesized systematic reviews with meta-analyses of observational studies (2017-02-01 to 2025-03-31) assessing sociodemographic, parental, perinatal, and later antecedents for ICD/DSM non-organic psychotic disorder diagnoses. It updates and grades evidence for risk and protective factors to support personalized prognosis and prevention planning. Clinically, the resulting evidence atlas can guide targeted early identification and prevention strategies for psychosis based on empirically supported factors.

Aymerich C, De Prisco M, Melillo A et al. · World psychiatry : official journal of the World Psychiatric Association (WPA) · (2026) · View on PubMed ↗

Cumulative Incidence and Prevalence of Autism Spectrum Disorder.

This JAMA Pediatrics study estimated 7-year cumulative incidence and prevalence of autism spectrum disorder (ASD) across 12 consecutive birth cohorts in South Korea using prospective population-based screening and diagnostic assessment. It tested whether ASD incidence/prevalence at age 7 changed over time while minimizing biases from administrative or service-based ascertainment. The scientific significance is that it provides more robust, cohort-based epidemiologic estimates of ASD trends relevant for public health planning.

Kim YS, Liu X, Chang J et al. · JAMA pediatrics · (2026) · View on PubMed ↗

Idiopathic Normal Pressure Hydrocephalus: A Review.

This review studied idiopathic normal pressure hydrocephalus (iNPH) in older adults, focusing on how cerebrospinal fluid (CSF) circulation, vascular dysfunction, and white matter injury interact to produce gait impairment, urinary dysfunction, and cognitive decline. It found that iNPH is a multifactorial condition without a known antecedent event (unlike secondary NPH) and that these interacting mechanisms likely drive disease progression. Clinically, the synthesis supports more mechanism-informed approaches to diagnosis and treatment selection for the ~1%–4% of people aged ≥65 years and ~6%–8% aged ≥80 years who are affected.

Maroufi SF, Yasar S, Moghekar A et al. · JAMA · (2026) · View on PubMed ↗

Perceived Importance of Good Death Components Among Patients With Advanced Cancer and Family Caregivers.

This cross-sectional study examined perceived importance of components of a “good death” among adults with stage III/IV cancer and their family caregivers in Hong Kong, mainland China, and Turkey using the 54-item Good Death Inventory. The key finding was that priorities for good-death components differed across settings and that patient–caregiver differences and setting-by-role interactions were assessed. The results are significant for palliative care policy and interventions by identifying culturally and role-specific targets for advance care planning.

Abu-Odah H, Can G, Plakas S et al. · JAMA network open · (2026) · View on PubMed ↗

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Endocrine/Metabolic Disorders & Obesity/Diabetes Care

Consensus-based clinical and research recommendations for use of glucagon-like peptide-1 receptor agonists in the context of eating disorders: a modified Delphi study.

This modified Delphi consensus study (three rounds; N=45 including diabetes/obesity/ED experts and people with lived experience) developed clinical and research recommendations for using glucagon-like peptide-1 receptor agonists (GLP-1RAs) in the context of eating disorders. The panel reached ≥70% consensus on structured guidance addressing concerns that GLP-1RAs’ appetite suppression and weight loss could worsen or precipitate eating disorder symptoms. The recommendations aim to standardize safer prescribing and to define research priorities where evidence is currently limited or inconsistent.

Keshen A, Koning E, Allison KC et al. · World psychiatry : official journal of the World Psychiatric Association (WPA) · (2026) · View on PubMed ↗

Real-World Evidence for Existing Anti-Obesity Therapies-The Realities of Treatment Adherence, Tolerability, Access and Patient Satisfaction.

This narrative review synthesized real-world evidence on adherence, tolerability, access, and patient satisfaction for existing anti-obesity interventions, with emphasis on incretin-based pharmacotherapy, across lifestyle programs, pharmacotherapy, metabolic bariatric surgery, and endoscopic procedures. It finds that real-world outcomes are often attenuated compared with randomized trials due to barriers such as limited access, tolerability issues, and insufficient long-term support, which can affect adherence and patient-reported satisfaction. Clinically, the review highlights where health systems and treatment strategies must improve to translate anti-obesity efficacy into sustained real-world effectiveness.

Kassem S · Diabetes, obesity & metabolism · (2026) · View on PubMed ↗

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Computational/AI Methods in Medicine (pathology, imaging, foundation models)

A clinically-oriented foundation model for intraoperative pathology.

This study introduced CRISP, a clinically oriented foundation model for intraoperative pathology built from >100,000 frozen sections across ten medical centers and evaluated on >15,000 intraoperative slides. CRISP was designed to provide robust intraoperative support for pathology and was assessed using retrospective and prospective-like validation settings (nearly 100 retrospective cohorts reported). The clinical significance is improved feasibility and reliability of computational pathology in surgical workflows, addressing the current bottleneck of limited high-quality frozen-section data and diagnostic complexity.

Zhao Z, Zhou F, Li R et al. · Nature medicine · (2026) · View on PubMed ↗

Prediction of maternal and infant outcomes from longitudinal electronic health records with a Mother-Child AI agent.

This study developed MoChiAgent, an LLM-based Mother-Child AI agent that integrates longitudinal electronic health record (EHR) data (including routine labs) to forecast maternal and infant outcomes. Using MoChiFormer, the model was internally evaluated on 4,401,599 longitudinal visits and externally validated on independent cohorts with 263,452 and 23,192 visits, respectively, and it reconstructs missing laboratory data to enable prediction. The significance is a scalable, lower-cost approach to predicting pregnancy and infant disease risk from routine EHR streams, potentially improving prenatal and postnatal care planning.

Liu S, Zheng W, Kang J et al. · Nature medicine · (2026) · View on PubMed ↗

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Transthyretin Amyloid Cardiomyopathy (ATTR-CM) Therapies

Eplontersen with and without background transthyretin stabilizers in transthyretin amyloid cardiomyopathy: secondary analysis of a phase 3, randomized controlled trial.

This secondary analysis of the phase 3 CARDIO-TTRansform randomized controlled trial evaluated eplontersen (a TTR gene silencer; 45 mg every 4 weeks) versus placebo in transthyretin amyloid cardiomyopathy (ATTR-CM), stratifying by background use of TTR stabilizers. Among 1,432 patients, 57% were on TTR stabilizers at baseline, and the analysis assessed the incremental effect of eplontersen with versus without stabilizer therapy. Clinically, clarifying whether eplontersen adds benefit on top of TTR stabilizers informs optimal combination treatment strategies for ATTR-CM.

García-Pavía P, Cappelli F, Davis MK et al. · Nature medicine · (2026) · View on PubMed ↗

Use of Sotatercept in France since Its Availability in June 2024: A Nationwide Study from the French Health Data System (SNDS).

This nationwide French real-world study used the French Health Data System (SNDS) to characterize early access use of sotatercept, a first-in-class fusion protein, in pulmonary arterial hypertension (PAH) since its availability in June 2024. The key finding was a description of treated patient characteristics, real-world administration patterns, and associated changes in background PAH therapy as eligibility criteria broadened over time. This is significant for understanding how sotatercept is implemented outside trials and how it influences concomitant PAH treatment in routine care.

Charifa N, Weill A, Zureik M et al. · Drugs - real world outcomes · (2026) · View on PubMed ↗

A trial emulation study indirectly comparing tafamidis and acoramidis in transthyretin amyloid cardiomyopathy: the ReplicATTR study.

This trial emulation study used real-world data from TriNetX (2019–2024) to indirectly compare acoramidis versus tafamidis for all-cause mortality in transthyretin amyloid cardiomyopathy, emulating eligibility criteria from the ATTR-ACT and ATTRibute-CM trials. The key finding was an indirect treatment comparison suggesting differences in 42-month all-cause mortality between acoramidis and tafamidis after calibration to trial outcomes. Clinically, this provides comparative effectiveness evidence to support decision-making between transthyretin stabilizers when head-to-head randomized data are limited.

Debonnaire P, Zwetsloot PP, Pfister R et al. · Journal of comparative effectiveness research · (2026) · View on PubMed ↗ · Free PDF ↗

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Genome Editing & Gene Therapy (including base editing, iPSC/organoids)

Highly efficient base editing at PCSK9 and normal human embryo development.

This study evaluated Cas9 base editing in human embryos by delivering ABE8e-V106W protein at fertilization to introduce base edits at PCSK9 and HBG loci. Editing occurred at all PCSK9 alleles, embryos developed to the blastocyst stage, and homozygous edited stem cell lines were derived without detectable insertions or deletions, though rare on-target chromosome breakage and chromosomal abnormalities were observed. The scientific significance is demonstrating high-efficiency base editing compatible with early human development while highlighting residual genotoxic risks relevant to genome correction safety.

Jerabek S, Jung C, Kappy M et al. · Nature · (2026) · View on PubMed ↗

Base editing rescues a hereditary motor neuron disease in mouse and patient-derived iPSC organoid models.

This 2026 study tested base editing as a gene therapy approach for hereditary motor neuron disease using both mouse models and patient-derived iPSC organoid models. It targeted the P285L single-nucleotide variant in the TRK-fused gene (TFG) and identified an optimal adenine base editor to rescue disease phenotypes (full methods/results truncated). The work provides proof-of-concept that base editing can correct a pathogenic variant and restore function in both in vivo and patient-derived organoid systems.

Imamura K, Yoshioka S, Kamizato K et al. · Molecular therapy. Advances · (2026) · View on PubMed ↗

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Methodology, Guidelines & Consensus (biomarkers, clinical guidelines, protocols)

The Management of Type 1 Diabetes in Adults. The Updated 2026 Consensus Report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD).

This 2026 consensus report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) studied evidence-based management strategies for adults with type 1 diabetes. It emphasizes integration of new diabetes technologies and revises all sections with updated evidence, including interventions aimed at delaying stage 3 type 1 diabetes and expanded screening for long-term complications, obesity, and cardiovascular risk factors. Clinically, it provides updated, technology-forward guidance to improve outcomes and risk management across the adult type 1 diabetes care continuum.

Holt RIG, DeVries JH, Hess-Fischl A et al. · Diabetes care · (2026) · View on PubMed ↗

The European Multidisciplinary Evidence-Based Guideline on Pancreatic Cancer: Methodological Protocol.

This methodological protocol describes how the European Multidisciplinary Evidence-Based Guideline on Pancreatic Cancer will be developed for clinicians, researchers, and patients across Europe. It will synthesize state-of-the-art evidence and expert opinion to address pancreatic cancer topics where consensus is lacking and to explicitly identify knowledge gaps. The guideline framework is significant because it standardizes evidence-to-recommendation processes to improve decision-making and future research prioritization in a highly lethal cancer.

Leeuwenburgh LC, Holze M, Akhoundzadeh D et al. · Clinical and public health guidelines · (2026) · View on PubMed ↗

The diagnostic biomarker problem in amyotrophic lateral sclerosis.

This article studied the concept and requirements of diagnostic biomarkers in amyotrophic lateral sclerosis (ALS), focusing on how biomarker performance should be defined for use when diagnosis is uncertain. It emphasizes that useful diagnostic biomarkers must achieve high positive predictive value and/or high negative predictive value at the time of clinical uncertainty, rather than being evaluated only by other metrics. The significance is that it provides a practical framework to reduce diagnostic delay in ALS by improving how biomarker studies are designed and interpreted.

Benatar M, Wuu J, Turner MR et al. · Brain : a journal of neurology · (2026) · View on PubMed ↗

A practical guide to studying genome function using single-molecule genomics.

This Expert Recommendation article reviewed and provided a practical guide for studying genome function using single-molecule genomics (SMG) techniques that profile regulatory factor activity on individual DNA molecules. The key finding is that SMG can quantify heterogeneity and co-occurrence of regulatory events—such as epigenetic modifications, transcription factor binding, and chromatin organization—while capturing chromatin interaction dynamics not measurable by conventional bulk genomics. Scientifically, this positions SMG as a workflow foundation for mechanistic, single-molecule dissection of genome regulation.

Krebs AR, Altemose N, Churchman LS et al. · Nature reviews. Molecular cell biology · (2026) · View on PubMed ↗

Evaluation and Management of Anemia in Chronic Kidney Disease: Synopsis of the Kidney Disease: Improving Global Outcomes 2026 Clinical Practice Guideline.

This guideline synopsis summarized the 2026 Kidney Disease: Improving Global Outcomes (KDIGO) clinical practice guideline for anemia management in chronic kidney disease (CKD). It covers anemia diagnosis and treatment with iron therapy, erythropoiesis-stimulating agents (ESAs), hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHIs), and red blood cell (RBC) transfusions, based on evidence reviews through October 2024. The update standardizes evidence-based care to improve anemia outcomes and reduce treatment variability in CKD.

Hedayati SS, Babitt JL, Berns JS et al. · Annals of internal medicine · (2026) · View on PubMed ↗

Defining and managing high-risk acute myeloid leukemia (AML) in 2026.

This review studied how to define and manage high-risk acute myeloid leukemia (AML) in 2026, contrasting traditional static, genetics-centered risk definitions (e.g., complex cytogenetics, TP53 alterations, and therapy-related/secondary-associated mutations) with emerging dynamic models. The key finding was that risk assessment is increasingly shaped by treatment intensity, patient fitness, measurable residual disease (MRD), and evolutionary context rather than baseline genetics alone. Clinically, this supports more adaptive risk stratification to guide therapy selection and monitoring in high-risk AML.

Alibrahim MN, Elsayed MA, Alqahtani AN et al. · Annals of hematology · (2026) · View on PubMed ↗

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Cardiac Repair, Immune Remodeling & Infection-Driven Inflammation

Intestinal Serotonergic Vagal Signaling as a Mediator of Microbiota-Induced Hypertension.

This 2026 study investigated how intestinal serotonergic vagal signaling mediates microbiota-induced hypertension using fecal microbiota transplantation between normotensive and hypertensive rats and an intersectional genetic approach targeting serotonin receptors (details truncated). It found that gut microbiota can drive hypertension through a serotonin–vagal signaling pathway rather than solely through cardiac, renal, or cerebral mechanisms. Scientifically and clinically, it identifies a gut–brain serotonergic circuit as a potential target to overcome microbiota-associated, treatment-resistant hypertension.

de Araujo A, Sree Kumar H, Yang T et al. · Circulation · (2026) · View on PubMed ↗

CCND1 Mitigates Ischemia-Induced Pathological Cardiac Remodeling by Promoting Cardiac Monocyte-Derived Macrophage Transition to a Reparative Phenotype.

This 2026 study examined whether CCND1 (cyclin D1) influences post–myocardial infarction (MI) immune remodeling by promoting monocyte-derived macrophage transition to a reparative phenotype. It found that CCND1 mitigated ischemia-induced pathological cardiac remodeling by steering recruited monocyte-derived macrophages toward reparative states during the postinfarct inflammatory-to-reparative transition (human peripheral blood monocytes/macrophage methods truncated). The work highlights CCND1 as a potential immunomodulatory target to improve cardiac repair and long-term outcomes after MI.

Wang C, Han H, Li K et al. · Circulation · (2026) · View on PubMed ↗

Cytomegalovirus Latency Fuels Inflammation Following Myocardial Infarction.

This experimental study examined how latent murine cytomegalovirus (CMV) infection affects cardiac immune cell dynamics at baseline and during post-myocardial infarction (MI) repair in C57BL/6J mice. Using spectral flow cytometry plus bulk and single-cell RNA/T-cell receptor (TCR) sequencing, the authors found that CMV latency fueled post-MI inflammation by reshaping immune responses during cardiac repair. These findings mechanistically connect CMV latency to adverse cardiovascular remodeling and suggest that targeting latent CMV–driven inflammation could be a therapeutic strategy after MI.

Dapergola E, Šustić M, Ashour D et al. · Circulation research · (2026) · View on PubMed ↗ · Free PDF ↗

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Respiratory Disease (COPD/RSV/OSA-related) & Pulmonary Therapeutics

Efficacy of Biologics in Patients with Moderate to Very Severe COPD: A Systematic Review.

This 2026 systematic review studied the efficacy of biologics in patients with moderate to very severe chronic obstructive pulmonary disease (COPD), focusing on randomized phase 2/3 trials published up to July 9, 2025. It found that many biologics reduce acute exacerbations of COPD (AECOPD), particularly in subgroups with elevated blood eosinophil counts (BEC), and assessed effects on pre-bronchodilator FEV1 and St George’s Respiratory Questionnaire (SGRQ/SGRQ-C) scores. Clinically, it synthesizes comparative evidence to support biologic selection and biomarker-driven treatment strategies in COPD.

Brightling CE, Rabe KF, Singh D et al. · International journal of chronic obstructive pulmonary disease · (2026) · View on PubMed ↗

Obstructive sleep apnea, GLP-1 receptor agonist pharmacotherapy, and the oral microbiome: competing biological influences and implications for oral health monitoring.

This review studied how obstructive sleep apnea (OSA) and GLP-1 receptor agonist pharmacotherapy may interact through the oral microbiome and oral health monitoring, including implications of newer OSA-related approvals such as tirzepatide. The key finding was that OSA-associated oral microbiome dysbiosis can arise from multiple simultaneous pathways (intermittent hypoxia immune dysregulation, mouth breathing/salivary desiccation, elevated salivary glucose, reflux acid challenge, and HPA-axis effects), which may compete with or be modified by GLP-1RA effects. Clinically, it highlights the need to consider these competing biological influences when monitoring oral health in patients treated with GLP-1RAs for OSA.

Comisi JC · Clinical oral investigations · (2026) · View on PubMed ↗

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Inflammatory Bowel Disease (IBD) Targeted Therapies

Targeted Therapies in Inflammatory Bowel Disease: Mechanisms, Comparative Evidence, and Clinical Translation.

This narrative review examined the mechanistic rationale, comparative clinical evidence, and translational considerations for approved and emerging targeted therapies in adult inflammatory bowel disease (Crohn’s disease and ulcerative colitis). It synthesizes evidence from 2021–March 2026 to compare how different targeted pathways perform clinically and how they may be translated into practice. The significance lies in clarifying which targeted mechanisms have the strongest comparative support for CD/UC and where translational gaps remain for future therapy development.

Pavel C, Popa A, Ilie M et al. · Journal of clinical medicine · (2026) · View on PubMed ↗

Guselkumab in Inflammatory Bowel Disease: Mechanism, Clinical Efficacy, Safety, and Treatment Positioning.

This review focused on guselkumab, an IL-23p19 monoclonal antibody, in the treatment of patients with inflammatory bowel disease (Crohn’s disease and ulcerative colitis). It reports that guselkumab blocks IL-23 binding to the IL-23 receptor and highlights clinical efficacy and safety positioning, including the distinctive fully subcutaneous induction regimen and emerging phase III signals for perianal Crohn’s disease. The clinical significance is that it frames where guselkumab fits among IL-23 inhibitors and other IBD options based on mechanism and trial-derived performance.

White L, Sharma E, Limdi J et al. · Journal of clinical medicine · (2026) · View on PubMed ↗

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Reproductive Toxicology & Environmental Exposures

Molecular Mechanisms of Endocrine-Disrupting Chemicals and Emerging-Pollutant Toxicity in Human Reproduction: From Xenobiotic Exposure to Fertility Impairment and Reproductive Carcinogenesis.

This review examined how endocrine-disrupting chemicals (EDCs) and emerging pollutants affect human reproduction, linking xenobiotic exposure to fertility impairment and reproductive carcinogenesis. It argues that diverse chemical classes (e.g., phthalates, bisphenols, PFAS, pesticides, PCBs/dioxins, flame retardants, PPCPs, and micro/nanoplastics) share convergent molecular toxicology mechanisms that can drive hormone-dependent reproductive cancer risk. Scientifically, the proposed unified latency model helps integrate reproductive toxicology and cancer biology to guide risk assessment and mechanistic research.

El Beaino Z, Ayoubi JM, Hamamah S · International journal of molecular sciences · (2026) · View on PubMed ↗

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Cancer Adjuvant Therapy Personalization (ctDNA-guided) & Treatment De-escalation

Circulating tumor DNA-guided de-escalation or escalation of adjuvant therapy in high-risk stage II and stage III colon cancer: the phase 2 PEGASUS trial.

This phase 2 PEGASUS trial studied a ctDNA-guided adaptive de-escalation or escalation strategy in patients with resected microsatellite-stable, high-risk stage II (T4N0) or stage III colon cancer. ctDNA-positive patients received CAPOX for 3 months then escalated to FOLFIRI for 6 months if ctDNA remained positive, while confirmed ctDNA-negative patients received 6 months of capecitabine, aiming to reduce overtreatment while maintaining relapse control. The significance is that it tests whether post-surgery ctDNA status can personalize adjuvant chemotherapy intensity to balance toxicity and recurrence risk.

Marsoni S, Montagut C, Pietrantonio F et al. · Nature cancer · (2026) · View on PubMed ↗

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Epigenetics & Chromatin Regulation

Cryo-EM structure, enzymatic activity and genome targeting of canonical PRC1.

The study determined the cryo-electron microscopy structure and functional mechanism of the human canonical polycomb repressive complex 1 (cPRC1) holocomplex containing RING1B, BMI1, PHC2, and CBX7 bound to an H3K27me3-modified mononucleosome with the ubiquitin-conjugating enzyme UBCH5C. The authors found a compact, integrated architecture that positions UBCH5C on the nucleosome to enable efficient monoubiquitination of histone H2A at K119, with an interface formed by RING1B, BMI1, and PHC2 that is conserved in Drosophila. This mechanistic structural insight clarifies how cPRC1 enforces developmental gene repression and provides a conserved framework for targeting PRC1-dependent epigenetic regulation.

Ciapponi M, Cafiso M, Schkölziger S et al. · Nature structural & molecular biology · (2026) · View on PubMed ↗

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Acute Coronary Syndromes & Antithrombotic Strategies

APOE-stratified genome-wide association analyses provide insights into the genetic etiology of Alzheimers’s disease.

The study performed APOE-stratified genome-wide association analyses to dissect the genetic architecture of late-onset Alzheimer’s disease and related dementias in the context of APOE ε2/ε3/ε4 polymorphisms. By stratifying by APOE genotype, the authors aimed to clarify how risk loci and mechanisms differ across ε4 versus ε2 carriers, addressing the longstanding gap in understanding the biological basis of APOE-driven dementia risk. This approach can improve etiologic interpretation of AD GWAS signals and inform more genotype-aware therapeutic strategies, especially given differential responses to anti-amyloid treatments.

Thomassen JQ, Leonard H, Ulms B et al. · Nature genetics · (2026) · View on PubMed ↗

Ultrashort vs Standard-Duration Dual Antiplatelet Therapy in Acute Coronary Syndrome Patients Undergoing PCI: A Meta-Analysis.

This meta-analysis compared ultrashort (≤1-month) versus standard-duration dual antiplatelet therapy (DAPT) in acute coronary syndrome patients undergoing percutaneous coronary intervention (PCI) using randomized controlled trials. Ultrashort DAPT was evaluated for effects on major adverse cardiac and cerebrovascular events (MACCE), major bleeding, and net adverse clinical events (NACE), with prespecified subgroup analyses by ethnicity (East Asian vs non-East Asian). The results inform optimal DAPT duration strategies to balance ischemic protection and bleeding risk after PCI in ACS.

Hendrianus H, Gorog DA, Tantry US et al. · JACC. Cardiovascular interventions · (2026) · View on PubMed ↗

Clinical Management of Myocardial Infarction.

This article reviews the pathophysiology and clinical management of myocardial infarction (MI) in patients with coronary artery disease, focusing on atherothrombosis from plaque rupture/erosion and the resulting coagulation and platelet activation. It highlights that protocolized, timely revascularization is a key milestone and frames current acute and long-term strategies to reduce mortality. The review is clinically significant because it consolidates evidence-based approaches for improving outcomes in a leading global cause of death.

Landi A, Malik FTN, Chieffo A et al. · Circulation · (2026) · View on PubMed ↗

Old drug with new application: spironolactone suppresses Panx 1-mediated Ca2+ influx to attenuate inflammation-driven neutral lipid accumulation in early atherosclerosis.

This mechanistic study investigated how spironolactone (SP) suppresses Panx1 (pannexin 1)-mediated Ca2+ influx to attenuate inflammation-driven neutral lipid accumulation in early atherosclerosis, focusing on endothelial cells (ECs). The key finding was that SP’s anti-inflammatory effect involves Panx1-dependent regulation of Ca2+ entry, linking a known drug target to a specific inflammatory lipid-accumulation pathway. This is significant because it suggests a targeted, inflammation-focused mechanism for repurposing spironolactone to slow early atherosclerotic progression.

Yang Y, Gu T, Zheng M et al. · Inflammation research : official journal of the European Histamine Research Society … [et al.] · (2026) · View on PubMed ↗

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Digital Health, Wearables & Real-World Evidence Implementation

Outcomes of elacestrant in patients with ER-positive, HER2-negative, ESR1-mutated metastatic breast cancer who received prior endocrine therapy and cyclin-dependent kinase inhibitor in a real-world setting.

This real-world outcomes study assessed elacestrant in patients with ER-positive, HER2-negative, ESR1-mutated metastatic breast cancer who had received prior endocrine therapy and a cyclin-dependent kinase inhibitor (CDK4/6i). Using Komodo Research Dataset claims linked with Foundation Medicine clinical-genomics data (N=281), the primary endpoint was median time-to-next-treatment (mTTNT). The findings evaluate how elacestrant performs in routine practice for ESR1-mutant disease after endocrine therapy and CDK4/6 inhibition.

Curigliano G, De Laurentiis M, Harbeck N et al. · ESMO open · (2026) · View on PubMed ↗

Health Literacy and Capecitabine Adherence in a Remote Monitoring Pilot Trial for Breast Cancer: Post Hoc Exploratory Analysis.

This post hoc exploratory analysis evaluated whether health literacy was associated with adherence to oral capecitabine and whether it modified the effectiveness of a remote monitoring intervention in a remote monitoring pilot trial for breast cancer patients. The study found that lower health literacy was linked to worse capecitabine adherence and that the remote monitoring approach helped mitigate adherence problems, with differential benefit by health literacy level. These findings support tailoring adherence support for capecitabine dosing schedules using remote monitoring, especially for patients with limited health literacy.

Hernandez S, Meisel J, Sadigh G et al. · JMIR formative research · (2026) · View on PubMed ↗

Bidirectional Associations Between Autonomic Function, Sleep Quality, and Daily Fatigue and Energy Symptoms in Long COVID: Longitudinal Digital Health Study.

This longitudinal digital health study used Fitbit Inspire 3 wearable monitoring in 14 individuals with long COVID to test bidirectional, within-person relationships between objectively measured sleep quality, nocturnal heart rate variability (HRV), and daily fatigue/energy symptoms. Daily fatigue/energy levels predicted subsequent sleep and autonomic recovery, and sleep/HRV also predicted next-day fatigue/energy, demonstrating reciprocal temporal dynamics. These findings highlight modifiable daily sleep-autonomic pathways that may be targeted to improve fatigue in long COVID.

Aboagye NY, R Baker M, Baker K et al. · JMIR cardio · (2026) · View on PubMed ↗

Treatment Patterns and Outcomes After Recurrence Following Adjuvant Nivolumab for Urothelial Carcinoma: An AGEHA Real-World Study.

This real-world retrospective AGEHA database study evaluated post-recurrence treatment patterns and outcomes after adjuvant nivolumab for urothelial carcinoma in patients who had undergone radical cystectomy or nephroureterectomy. Among 141 patients, 40 developed recurrence, and first-line post-recurrence therapy was categorized (including enfortumab vedotin plus pembrolizumab [EVP], enfortumab vedotin [EV], non-EV regimens, or no systemic therapy), with overall survival measured from recurrence and progression-free survival from treatment initiation. The findings characterize how nivolumab-treated patients are managed after relapse and provide outcome benchmarks to guide subsequent therapy selection in routine practice.

Ogawa I, Narita T, Shinohara M et al. · International journal of urology : official journal of the Japanese Urological Association · (2026) · View on PubMed ↗

Adoption of Adjunctive Azithromycin for Unscheduled Cesarean Delivery and Postpartum Infections.

This JAMA study assessed real-world adoption of adjunctive azithromycin for unscheduled cesarean delivery and postpartum infections by analyzing US pregnant persons using Epic Cosmos and applying a difference-in-differences design. It evaluated whether practice patterns followed trial evidence and characterized postpartum infection trends after implementation in routine care. The clinical significance is that it informs how effectively evidence-based antibiotic prophylaxis translates into population-level outcomes.

Freret TS, Litman E, Wen T et al. · JAMA · (2026) · View on PubMed ↗

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Musculoskeletal Biomechanics & Rehabilitation

Immediate Self-Rehabilitation With Versus Without Sling Immobilization After Open Latarjet Procedures for Recurrent Anterior Shoulder Instability: A Randomized Controlled Trial.

This monocentric randomized controlled trial compared immediate self-rehabilitation with versus without sling immobilization after open Latarjet procedures for recurrent anterior shoulder instability in 86 patients (median age 26). The study assessed patient-reported outcomes, motion-capture kinematics, and CT imaging at baseline and 6 months, testing whether avoiding sling immobilization improves functional recovery. The results are intended to inform postoperative rehabilitation protocols by clarifying whether sling-free early mobilization reduces immobilization-related harms while maintaining structural and functional outcomes.

Goetti P, Bothorel H, Martinho T et al. · The Journal of bone and joint surgery. American volume · (2026) · View on PubMed ↗

Neuromechanical Determinants of Muscle-Specific Hamstring Damage and Hypertrophy across Exercises: An EMG-Informed Modeling Approach.

This study used neuromusculoskeletal modeling to compare neuromechanical determinants of acute hamstring muscle damage and chronic hypertrophy across exercises (isokinetic seated leg curl, Nordic hamstring exercise, and stiff-leg variants), estimating activation, operating length, and force for semimembranosus, semitendinosus, and biceps femoris long head. It found that exercise-specific neuromechanical features govern which hamstring muscle is most affected and which adapts most, linking differences in activation/length/force to damage and hypertrophy patterns. The findings are scientifically significant for tailoring hamstring training to target specific muscles and potentially reduce injury risk.

Morin T, Doguet V, Mauget A et al. · Medicine and science in sports and exercise · (2026) · View on PubMed ↗

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Autosomal Dominant Polycystic Kidney Disease (ADPKD) Therapeutics & Cilia Biology

CDK4/6 Inhibitor Abemaciclib Arrests and Reverses Kidney Cyst Progression in Preclinical Models of Autosomal Dominant Polycystic Kidney Disease.

This preclinical study tested the CDK4/6 inhibitor abemaciclib in models of autosomal dominant polycystic kidney disease (ADPKD) to determine whether CDK6 inhibition can restore ciliary polycystin function and slow cyst progression in vivo. Abemaciclib arrested and reversed kidney cyst progression and was mechanistically linked to cilia biology, building on prior evidence that CDK6 suppresses axonemal polyglutamylation to restrict ciliary polycystin abundance. The work is significant because it supports repurposing abemaciclib as a potentially more effective and better-tolerated therapeutic approach beyond tolvaptan for ADPKD.

Cao Y, Sun X, Huang Y et al. · Journal of the American Society of Nephrology : JASN · (2026) · View on PubMed ↗

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Chronic Kidney Disease & Cardiovascular Risk (ASCVD in CKD)

Atherosclerotic Cardiovascular Disease in CKD: Contemporary Insights into Pathogenesis, Diagnosis, and Management.

This review synthesized how atherosclerotic cardiovascular disease (ASCVD) develops and is managed in chronic kidney disease (CKD), emphasizing both traditional risk factors and CKD-specific mechanisms such as mineral/bone disorder with vascular calcification, chronic inflammation/oxidative stress, uremic toxicity, and atherogenic dyslipidemia. It highlights the bidirectional interaction between kidney and cardiovascular disease that drives high cardiovascular mortality in CKD. The scientific significance is that it provides a contemporary framework for improving diagnosis and treatment of ASCVD in CKD populations.

Correa S, Cuningham JW, Mc Causland FR · Clinical journal of the American Society of Nephrology : CJASN · (2026) · View on PubMed ↗

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Diabetic Kidney Disease & Macrophage Immunology

Spatially Distinct TREM2+ Macrophages Are Associated with Compartment-Specific Protection in Diabetic Kidney Disease.

This study investigated diabetic kidney disease (DKD) by integrating single-cell RNA sequencing, spatial transcriptomics, and reciprocal bone marrow transplantation in OVE26 diabetic mouse kidneys to map TREM2+ macrophage heterogeneity. It found that spatially distinct TREM2+ macrophage populations are associated with compartment-specific protection, implying functional specialization by anatomical localization and developmental origin. The clinical significance is that targeting or harnessing specific TREM2+ macrophage niches could become a precision strategy to mitigate DKD progression.

Fu J, Niu Y, Chang D et al. · Journal of the American Society of Nephrology : JASN · (2026) · View on PubMed ↗

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Cardiometabolic-Gut-Brain Axis (microbiome, inflammation, hypertension, PSD)

Integrated metagenomic and metabolomic analysis identifies severity-specific inflammatory and metabolic signatures in post-stroke depression.

This study integrated metagenomic sequencing, non-targeted metabolomics, and serum cytokine profiling to define severity-specific gut microbial, metabolic, and inflammatory signatures in post-stroke depression (PSD). In 91 patients with varying PSD severities and non-PSD controls, multi-omics network analysis and machine learning identified PSD-associated inflammatory and metabolic patterns, including altered gut microbiota features and cytokine profiles (e.g., IL-1β, IL-6, IL-10, IL-18, TNF-α, IFN-γ, and CRP). Scientifically, it provides candidate biomarkers and mechanistic links between gut ecology, systemic inflammation, and PSD severity that could inform future stratified interventions.

Chen W, Pan Y, Chen M et al. · Gut microbes · (2026) · View on PubMed ↗ · Free PDF ↗

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Generated automatically on September 16, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.