PubMed Trending Research Digest — July 22, 2026

Automated digest · 96 articles · 15 research areas · July 22, 2026

Overview

Across this week’s set of papers, a dominant theme is the move from descriptive biology to mechanism-linked targets—often by connecting upstream perturbations (metabolic rewiring, immune signaling, or stress responses) to downstream functional complexes, pathways, and clinically measurable outcomes. In oncology, multiple studies emphasize pathway-level control of metastasis and therapy response (e.g., metabolic–signaling axes, immune escape via innate/adaptive resistance programs, and mutation-driven remodeling of the ubiquitin–proteasome system). In neurodegeneration, several works advance biomarker and mechanistic frameworks—blood phospho-tau and proteomic signatures for early diagnosis/staging, plus refined views of neuroinflammatory cell states (microglial diversity) and specific molecular “seeding” fractions of amyloid-β.

A second major theme is translational and clinical decision support: randomized trials and cohort analyses span diverse conditions (aplastic anemia, COPD/CRSwNP, RSV prophylaxis, dementia prevention, surgical recovery, and cancer functional outcomes), while reviews and guidelines aim to standardize care (pain management in inflammatory arthritis, postoperative pain after hip arthroplasty, prone positioning in ARDS, and interpretation of low-dose CBD). Complementing these are method-focused advances—new biomarker assays, imaging/omics mapping strategies, and even portable QC tools for pharmaceutical manufacturing—highlighting how better measurement is increasingly treated as part of the therapeutic pipeline.

Finally, immune modulation and host-directed strategies recur across infectious disease and inflammatory settings. Studies map how viral entry/fusion phenotypes alter interferon resistance, how vitamin A/ATRA dampens fatal inflammatory cascades in SFTSV, and how innate immune signaling (NOD1/2, complement) can shape adaptive immunity, cancer therapy resistance, or early neuroinflammation in synucleinopathies. Together, the collection underscores a broader trend: targeting the host’s signaling networks—whether in tumors, lungs, brain, or systemic inflammation—may yield more durable benefits than focusing solely on single disease-specific molecules.

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Cancer metabolism & metastatic signaling

Complement dysregulation during the early phases of synucleinopathy.

This study investigated complement dysregulation during early synucleinopathy by using a rat α-synuclein pre-formed fibril (PFF) model to probe whether complement activation is triggered directly by pathological α-syn rather than only after overt neurodegeneration. The key finding was that complement cascade activation occurs during early phases of synucleinopathy, supporting a more direct link between α-syn pathology and neuroinflammatory mechanisms. Scientifically, it strengthens the rationale for targeting complement pathways early in Parkinson’s disease–related synucleinopathies.

Khan H, Gifford M, Kordbacheh A et al. · Acta neuropathologica · (2026) · View on PubMed ↗

Mitochondrial SLC25A46 Rewires Fatty Acid Oxidation to Promote Cell Proliferation and Ferroptosis Evasion in Ovarian Cancer by Stabilizing CACT.

This study examined the role of mitochondrial SLC25A46 in ovarian cancer, using mechanistic experiments to determine how SLC25A46 rewires fatty acid oxidation and affects ferroptosis sensitivity. The key finding was that SLC25A46 promoted ovarian cancer cell proliferation and ferroptosis evasion by stabilizing CACT (carnitine-acylcarnitine translocase) and enhancing fatty acid oxidation–driven ATP and NADPH production, including via protection from MARCHF5-related regulation. This is significant because it identifies the SLC25A46–CACT axis as a potential metabolic vulnerability and therapeutic target to counter ferroptosis resistance in ovarian cancer.

Gao Y, Hao J, Zhang X et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Inhibition of the Metalloproteinase ADAMTS5 Suppresses Colorectal Cancer Metastasis via the PEDF/Wnt/β-Catenin Pathway.

This mechanistic cancer study investigated the role of the metalloproteinase ADAMTS5 in colorectal cancer (CRC) metastasis and tested whether it acts through the PEDF/Wnt/β-catenin pathway. It found that ADAMTS5 is upregulated in CRC tissues and that inhibiting ADAMTS5 suppresses CRC metastasis by modulating PEDF/Wnt/β-catenin signaling. These data position ADAMTS5 as a therapeutic target and provide a pathway-level rationale for anti-metastatic strategies in CRC.

Sun X, Zhang H, Hu Y et al. · Cancer medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Hemoperfusion during extracorporeal membrane oxygenation: an updated systematic review and meta-analysis of 8,151 patients.

This systematic review and meta-analysis evaluated adults receiving extracorporeal membrane oxygenation (ECMO) with hemoperfusion (ECMO+HP) versus ECMO alone, across 8,151 patients, to determine effects on all-cause mortality and safety. The key finding is the pooled comparative efficacy and risk profile of adding hemoperfusion, with subgroup analyses by randomized vs non-randomized design, ECMO type (VA vs VV), and etiology (cardiogenic shock vs cardiac arrest). Clinically, the results inform whether hemoperfusion should be considered as an adjunct strategy during ECMO in specific adult patient subgroups.

Xie T, Yang C, Tao H et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

ADSL drives fumarate mediated scrib-rictor complex formation to promote metastasis dissemination in triple-negative breast cancer.

This study investigated how the metabolic enzyme ADSL drives fumarate-mediated SLC7A11/Scrib-Rictor complex formation to promote metastasis dissemination in triple-negative breast cancer (TNBC) using untargeted metabolomics, chemoproteomic succination profiling, interaction analyses, and in vivo metastasis models. The authors found that ADSL-dependent fumarate signaling promotes formation of the Scrib-Rictor complex, thereby enhancing metastatic dissemination in TNBC. These findings link a specific metabolic rewiring step (ADSL→fumarate→Scrib-Rictor complex) to metastatic biology, suggesting a potential metabolic-kinase complex axis as a therapeutic target in aggressive TNBC.

Fan Y, He X, Deng W et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer microenvironment & immune evasion

NOD1/2 signaling in macrophages drives adaptive immune resistance in cancer.

This work studied the role of NOD1/2 signaling in macrophages in adaptive immune resistance to cancer therapies using murine tumor models and mechanistic perturbations. Genetic ablation of NOD1/2 or RIPK2, and pharmacologic inhibition of the pathway, reduced resistance across multiple antitumor modalities including immune checkpoint blockade, adoptive T-cell therapy, and cytotoxic chemotherapy. The findings identify NOD1/2–RIPK2 macrophage signaling as a potential target to overcome therapy resistance in the tumor microenvironment.

Wei X, Yang L, Wang Y et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗

RNA exonuclease REXO4 resolves m6A-marked R-loops and suppresses anti-tumor immunity.

This Molecular Cell study investigated how the RNA exonuclease REXO4 resolves N6-methyladenosine (m6A)-marked R-loops by 3’-5’ exonucleolytic cleavage of the RNA strand within RNA-DNA hybrids in human cells. It found that m6A promotes REXO4 localization to R-loops, and that REXO4 loss increases DNA damage, triggers an interferon response, and enhances tumor immune infiltration, suppressing tumor growth in mice. These findings link R-loop/m6A biology to anti-tumor immunity and suggest REXO4 as a potential target for immunomodulatory cancer strategies.

Zhang J, Bao K, Hou Y et al. · Molecular cell · (2026) · View on PubMed ↗

Cigarette Smoke-Exposed Alveolar Epithelial Cell-Derived Exosomes Exacerbate Skeletal Muscle Dysfunction Through HDAC2 Signalling.

This experimental study investigated whether exosomes derived from cigarette smoke–exposed alveolar epithelial cells drive skeletal muscle dysfunction in the context of COPD, with emphasis on histone deacetylase 2 (HDAC2) signaling. It found that blocking exosome signaling with the inhibitor GW4869 mitigated cigarette smoke–induced muscle injury and implicated HDAC2 as a key downstream pathway. Scientifically, it supports a mechanism in which epithelial exosome cargo modulates HDAC2-dependent inflammatory transcription to worsen COPD-related sarcopenia/skeletal muscle dysfunction.

Li C, Ou M, Jiang G et al. · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗ · Free PDF ↗

Pan-cancer proteogenomic interrogation of the ubiquitin-proteasome system.

This pan-cancer study used harmonized proteogenomic data from up to 11 CPTAC cohorts to interrogate how somatic mutations remodel the ubiquitin-proteasome system (UPS) at the protein level, focusing on UPS protein dysregulation and mutation-driven remodeling (notably TP53 loss). It found that mRNA levels poorly predict UPS protein abundance, that a recurrent set of E3 ligases is dysregulated across cancers, and that somatic mutations generate coherent UPS protein quantitative trait locus (pQTL) signatures. These findings support mutation-informed UPS targeting by showing that driver alterations—especially TP53 loss—reshape UPS composition in ways not captured by transcriptomics alone.

González-Robles TJ, Khan M, Sastourné P et al. · Cell death and differentiation · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Exosomes in cancer drug resistance: dual roles in therapy failure and emerging precision therapeutics.

This translational review described how tumor-derived exosomes contribute to cancer drug resistance while also being developed as precision-therapeutic tools, proposing an “exosome paradox.” The key finding is that exosomal cargo—including proteins such as P-gp and PD-L1, nucleic acids such as miR-21 and lncRNA H19, and lipids/metabolites—remodels the tumor microenvironment and activates pathways like PI3K/AKT and MAPK to promote therapy failure and immune evasion. The significance is that understanding exosome-mediated resistance mechanisms can guide both biomarker strategies and exosome-based therapeutic design.

Tegegne BA, Belew H, Teffera ZH et al. · Cancer cell international · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer therapeutics (clinical trials & approvals)

First CAR T-Cell Therapy Approved for Solid Tumors.

China approved satricabtagene autoleucel (satri-cel), a claudin 18.2–targeted, HER2-negative solid-tumor CAR T-cell therapy, for patients with claudin 18.2-positive, HER2-negative gastric or gastro-esophageal junction cancer. The phase II trial underlying the approval reported increased progression-free survival and overall survival with the CAR T cells. This regulatory milestone supports CAR T-cell expansion into solid tumors but highlights the need for further studies to improve efficacy and durability in this setting.

Cancer discovery · (2026) · View on PubMed ↗

Patient-reported Outcomes After Prostate Stereotactic Body Radiotherapy at 5 yr: Results from the PACE-B Trial.

In the phase 3, international PACE-B trial, patient-reported outcomes were assessed at 5 years in men with localized prostate cancer randomized to stereotactic body radiotherapy (SBRT) versus conventionally fractionated radiotherapy (CRT). At 5 years, urinary incontinence outcomes were favourable and comparable between SBRT and CRT, with leak-free rates reported as 64% (164/…). These long-term PROM data help clinicians and patients weigh functional side effects when choosing between SBRT and CRT for prostate cancer.

Cooper S, Patel J, Moore C et al. · European urology · (2026) · View on PubMed ↗

Phase 1/2 study of IMC-C103C, a T cell receptor bispecific (MAGE-A4×CD3) ImmTAC targeting MAGE-A4-expressing malignancies.

A phase 1/2 clinical study evaluated IMC-C103C, a T cell receptor bispecific ImmTAC (MAGE-A4×CD3) targeting an HLA-A02:01-presented MAGE-A4 peptide, in advanced solid tumors. In HLA-A02:01+ patients with previously treated disease, the trial assessed safety and preliminary anti-tumor activity using weekly intravenous dosing with step-up dosing and mTPI-2–guided dose escalation, alongside pharmacokinetics/pharmacodynamics and biomarker analyses. This design tests whether MAGE-A4–directed T cell engagement can produce clinically meaningful responses with an acceptable safety profile in MAGE-A4-expressing malignancies.

Sweis RF, Melero I, Davar D et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗

Beyond immune checkpoint blockade: T cell engagers and antibody-drug conjugates in cancer and autoimmune disease.

This review article synthesized preclinical and clinical evidence for next-generation immunotherapies beyond immune checkpoint blockade, focusing on T cell engagers (TCEs) and antibody-drug conjugates (ADCs) in cancer and immune-mediated inflammatory diseases (IMIDs). It concluded that TCEs can redirect cytotoxic T cells to target cells independently of MHC restriction, while ADCs deliver cytotoxic payloads via receptor-mediated internalization, offering strategies to overcome resistance and on-target toxicity limitations. These mechanistic insights help guide rational selection and development of TCE/ADC platforms for oncology and autoimmune indications.

Abdelaziz AM, Shokr MM · Biochemical pharmacology · (2026) · View on PubMed ↗

A bivalent molecular glue linking lysine acetyltransferases to oncogene-induced cell death.

This Cell study created lysine acetyltransferase (KAT)-based chemically induced proximity (CIP) tools, termed KAT-TCIPs, to induce oncogene-induced cell death in diffuse large B cell lymphoma by redirecting p300/CBP to activate cell-death networks repressed by BCL6. The lead KAT-TCIP reprogrammed the epigenome to initiate apoptosis, providing a targeted small-molecule approach to kill malignant cells driven by BCL6. This mechanistic strategy expands CIP-based cancer therapeutics beyond protein degradation and immune checkpoint paradigms.

Nix MN, Gourisankar S, Bowman KJ et al. · Cell · (2026) · View on PubMed ↗

Abemaciclib rechallenge after progression on abemaciclib plus endocrine therapy in patients with hormone receptor-positive HER2-negative metastatic breast cancer: results from the phase II again study (WJOG14220B).

This phase II again study evaluated abemaciclib rechallenge in hormone receptor-positive, HER2-negative metastatic breast cancer patients who progressed after prior abemaciclib plus endocrine therapy (ET), using switching strategies between aromatase inhibitor/tamoxifen (AI/TAM) and fulvestrant (FUL) while continuing abemaciclib. The key finding was that continuing abemaciclib with endocrine switching after progression produced measurable progression-free survival outcomes in this post–CDK4/6 inhibitor setting. This is clinically significant because it tests whether abemaciclib can be reused (“rechallenged”) to extend benefit for a subset of patients after initial CDK4/6 inhibitor failure.

Nishimura M, Kogawa T, Sugiyama K et al. · Breast cancer research and treatment · (2026) · View on PubMed ↗ · Free PDF ↗

Therapeutic targeting of CD47 using a tri-specific NK cell engager to inhibit multiple myeloma.

This preclinical study investigated therapeutic targeting of CD47 in multiple myeloma using a tri-specific NK cell engager designed to block CD47–SIRPα immune escape and enhance NK-mediated killing. The key finding was that CD47 blockade via the tri-specific engager inhibited multiple myeloma progression by promoting immune effector activity and overcoming resistance mechanisms associated with high CD47 expression. This is significant for immunotherapy development because it provides a rationale for multi-target NK engagers that simultaneously disrupt inhibitory signaling and improve anti-tumor phagocytosis/NK function.

Sumankan R, Sungwan P, Boonsatit N et al. · Cancer immunology, immunotherapy : CII · (2026) · View on PubMed ↗ · Free PDF ↗

TANGENT study design: a phase III, randomized study of emactuzumab for the treatment of tenosynovial giant cell tumors.

The TANGENT phase III randomized study evaluated emactuzumab, a CSF-1R inhibiting monoclonal antibody, in patients with tenosynovial giant cell tumors (TGCT) who were not adequately managed by surgery or had high post-surgical recurrence risk. The trial design targets tumor-associated macrophage reduction by blocking CSF-1R dimerization, aiming to improve clinically meaningful outcomes while addressing the limitations of long-term CSF-1R pathway inhibitor therapy. If successful, emactuzumab could provide a more effective and potentially less burdensome systemic option for unresectable or recurrent TGCT.

Gelderblom H, Palmerini E, van de Sande M et al. · Future oncology (London, England) · (2026) · View on PubMed ↗

Soluble high-molecular-weight amyloid-β species derived from amyloid-β-laden brains induce cerebral β-amyloidosis.

This in vivo study tested whether soluble high-molecular-weight amyloid-β (Aβ) species (>150 kDa) isolated from amyloid-β-laden brains of amyloid-β precursor protein transgenic mice or Alzheimer’s disease patients could seed pathology after intrahippocampal injection. The key finding was that these >150 kDa soluble Aβ species, prepared using size-exclusion chromatography, dramatically accelerated cerebral β-amyloidosis in transgenic mouse brains compared with controls. Scientifically, it identifies a specific Aβ molecular-weight fraction capable of acting as aggregation seeds, advancing understanding of how amyloid strains drive in vivo spreading.

Kashiwagi-Hakozaki M, Uchigami H, Naka Y et al. · Brain communications · (2026) · View on PubMed ↗ · Free PDF ↗

Temporal variability in outcomes of identical regimens across newly diagnosed myeloma trials: a systematic review.

This systematic review assessed temporal variability in progression-free survival (PFS) outcomes for identical regimens across newly diagnosed multiple myeloma trials, focusing on bortezomib/lenalidomide/dexamethasone (VRd) and lenalidomide/dexamethasone (Rd) arms without transplant. The key finding was that PFS for the same regimen varied across trials over time, and the review aimed to identify factors contributing to this variation, including informative censoring and diagnostic reclassification of smoldering myeloma after 2014. Scientifically and clinically, it cautions against naive cross-trial comparisons and highlights how evolving trial populations and censoring can bias apparent regimen efficacy.

Mohyuddin GR, Vaquera-Alfaro HA, Godara A et al. · EClinicalMedicine · (2026) · View on PubMed ↗ · Free PDF ↗

Redefining functional high-risk multiple myeloma in the context of upfront quadruplet therapy and autologous stem cell transplantation.

This cohort analysis studied how to redefine functional high-risk (FHR) multiple myeloma in the era of upfront quadruplet therapy plus autologous stem cell transplantation (QUAD + ASCT) using 310 newly diagnosed MM patients. The key finding was that the historical FHR definition (progression within 18 months with expected OS <2 years) may not optimally capture risk under modern QUAD + ASCT, prompting identification of alternative cutoff points associated with subsequent outcomes. Clinically, refining FHR criteria can improve risk stratification and guide treatment decisions for patients receiving contemporary induction and transplant strategies.

Ravi G, Dhakal B, Callander NS et al. · Cancer · (2026) · View on PubMed ↗

Dual-targeting pharmacological UFMylation inhibition reprograms tumor and immune microenvironments to achieve long-term glioblastoma regression.

This preclinical therapeutic study investigated dual-targeting pharmacological inhibition of UFMylation by targeting the UFMylation E3 ligase complex core protein DDRGK1 in glioblastoma models and its effects on tumor and immune microenvironments. It reported that osimertinib (via a previously unrecognized covalent mechanism) and the novel non-covalent inhibitor CP-24 disrupt the DDRGK1–UFL1 interaction, globally suppress UFMylation, inhibit ER-phagy, and drive ER stress leading to long-term glioblastoma regression. The work is significant because it provides first-in-class small-molecule UFMylation inhibitors that reprogram both tumor biology and immune contexture for durable glioblastoma control.

Tan P, Liu Z, Hu X et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer biomarkers & diagnostics (blood/omics/imaging)

Incidence, risk factors and tumor spectrum of second primary cancers after gastric cancer: a multicenter cohort study with long-term follow-up.

This multicenter MAGIS cohort study evaluated long-term incidence, risk factors, and tumor spectrum of second primary cancers (SPCs) in gastric cancer survivors who underwent curative-intent radical gastrectomy between 2007 and 2021. Using long-term follow-up and LASSO-penalized selection of clinical factors (with detection patterns and stage distribution assessed), the study characterized which survivor factors predicted SPC occurrence and how SPCs were detected over time. Clinically, the findings aim to refine surveillance strategies and risk stratification for SPCs after gastrectomy.

Gao X, Han W, Lu L et al. · BMC medicine · (2026) · View on PubMed ↗

Single-Cell Analysis of Residual Esophageal Squamous Cell Carcinoma After Neoadjuvant Immunochemotherapy Reveals TFAM-Mediated Immunoregulation in Dendritic Cells.

This study performed single-cell analysis on tumor microenvironments from 14 patients with esophageal squamous cell carcinoma (ESCC) who received neoadjuvant immunochemotherapy (nICT) to identify cellular programs linked to treatment response. The key finding was that TFAM-mediated immunoregulation in dendritic cells was associated with differential residual tumor outcomes after nICT, with NMF-derived immunosuppressive programs correlating with minimal or no pathological tumor regression. Scientifically and clinically, TFAM activity in dendritic cells may serve as a mechanistic biomarker and potential therapeutic target to improve nICT responsiveness in ESCC.

Chen L, Feng T, Zhou J et al. · Cancer research · (2026) · View on PubMed ↗

Immune checkpoint profiling of B7-H proteins predicts survival and treatment response in metastatic clear cell renal cell carcinoma.

This retrospective cohort study analyzed primary tumor specimens from 145 patients with metastatic clear cell renal cell carcinoma (ccRCC) to determine whether immune checkpoint profiling of B7-H family proteins predicts survival and treatment response. The key finding was that B7-H3, B7-H4, B7-H5, and B7-H7 expression showed compartmentalized intratumoral heterogeneity and that specific B7-H expression patterns were associated with tumor aggressiveness, treatment response, and long-term survival. Clinically, this suggests that B7-H profiling could help stratify metastatic ccRCC patients for prognosis and potential immunotherapy responsiveness.

Emaldi M, Rey-Iborra E, Mosteiro L et al. · The journal of pathology. Clinical research · (2026) · View on PubMed ↗ · Free PDF ↗

Anatomical and Histologic Response to Neoadjuvant Therapy: Recurrence Patterns Among Poor Responders. A Multi-institutional Observational Cohort Study.

This multi-institutional observational cohort study evaluated how anatomical response to neoadjuvant therapy (NAT), quantified by the Tumor Burden Score ratio (TBSr), and histologic response, assessed by Tumor Regression Grade (TRG), predict recurrence after hepatectomy for colorectal liver metastases (CRLM). It found that integrating TBSr with TRG improves characterization of recurrence patterns among poor responders. Clinically, this combined macroscopic–histologic framework could refine post-hepatectomy risk stratification and follow-up strategies for CRLM patients treated with NAT.

Baldo A, Akabane M, Elemosho A et al. · Annals of surgery · (2026) · View on PubMed ↗

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Cancer genomics & resistance mechanisms

Ligand regulation and function of preformed EGFR dimers.

This study used cryo-electron microscopy to determine the structural basis for how ligand regulation controls the function of preformed epidermal growth factor receptor (EGFR) dimers. The key finding was a detailed structural view showing how preformed EGFR dimers are stabilized and regulated, refining the classic ligand-induced dimerization model for EGFR activation. Scientifically, this provides a mechanistic framework that can inform rational design of EGFR-targeted therapies that exploit dimer conformational states.

Zuo Y, Schwartz HT, Walker K et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

α-fluoro-β-alanine functions as a β-arrestin1-biased ligand of S1PR2 to upregulate DPD expression in cancer cells.

This work investigated whether α-fluoro-β-alanine (FBAL), a catabolite of the chemotherapeutic 5-fluorouracil (5-FU), acts through sphingosine 1-phosphate receptor 2 (S1PR2) to regulate dihydropyrimidine dehydrogenase (DPD) in colorectal cancer cells. The key finding was that FBAL is a β-arrestin1-biased S1PR2 ligand that upregulates DPD expression via GRK6-dependent phosphorylation of S1PR2, thereby promoting 5-FU resistance. Clinically, targeting the FBAL–S1PR2–β-arrestin1/GRK6–DPD axis could help overcome or prevent 5-FU resistance in colorectal cancer.

Tan M, Shao H, Zhang X et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Precision Medicine in Pancreatic Cancer: Targeting KRAS and Beyond.

This review summarized precision medicine strategies in advanced/metastatic pancreatic cancer, focusing on targeting mutant KRAS and related pathways enabled by emerging KRAS inhibitors and trial evidence such as RASolute 302. The key finding is that KRAS inhibition has demonstrated clinically meaningful activity in metastatic pancreatic cancer, shifting more patients from “undruggable” biology toward actionable targeted therapy. This is significant because it reframes treatment paradigms beyond conventional chemotherapy by expanding the proportion of patients eligible for genotype-directed interventions.

Schürmann H, Park W, O’Kane GM et al. · Targeted oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Tailored strategies to overcome third-generation TKI resistance in EGFR-mutated non-small cell lung cancer.

This review article summarized evidence on tailored strategies to overcome resistance to third-generation EGFR tyrosine kinase inhibitors in EGFR-mutated non-small cell lung cancer (NSCLC). It organizes resistance mechanisms into on-target alterations (e.g., EGFR C797S and other secondary kinase domain mutations), off-target pathway activation (e.g., MET or HER2 amplification, RAS–MAPK signaling, oncogenic fusions), and neuroendocrine transformation to small-cell lung cancer. Clinically, it frames how molecular profiling can guide combination or switch strategies to counter specific resistance routes after third-generation TKI failure.

Saporita I, Farinea G, Lombardi E et al. · Expert opinion on therapeutic targets · (2026) · View on PubMed ↗

RNA modifications in cancer: regulators of tumor evolution and therapeutic response.

This review article summarized how RNA modifications (including m6A, m1A, m5C, m7G, pseudouridine, and A-to-I editing) regulate cancer evolution and therapeutic response through the epitranscriptomic network of writers, readers, and erasers. The key finding is that dysregulated RNA modification pathways control transcript stability and translation efficiency, thereby shaping tumor progression and treatment sensitivity/resistance. Scientifically, it consolidates mechanistic links between RNA modification biology and actionable therapeutic opportunities across cancer types.

Gu X, He Y, Xu Z et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Tumor evolution: signaling pathways, molecular mechanisms and therapeutic targets.

This review synthesized current knowledge on tumor evolution, emphasizing signaling pathways and molecular mechanisms that drive adaptive plasticity in heterogeneous cancers. The key finding is that advances such as high-throughput sequencing, single-cell and spatial omics, lineage tracing, computational modeling, and noninvasive biopsy enable dynamic characterization of evolutionary trajectories. The scientific significance is that these tools and pathways can be leveraged to identify therapeutic targets aligned with evolving tumor states.

Zhang KY, Zhu XZ, Yan YX et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer-targeted delivery & platform technologies

Targeted mRNA Delivery Using Bispecific Antibody-Lipid Nanoparticle Complexes.

This study developed and tested targeted mRNA delivery using bispecific antibody–lipid nanoparticle complexes (TbsAb-LNPs) designed to enrich uptake beyond liver for extrahepatic applications. The key finding was that the bispecific antibody targeting strategy enabled modeling of targeted uptake in vitro, addressing a major limitation of conventional lipid nanoparticles for tissue-specific delivery. Scientifically, it provides a platform approach for engineering targeted RNA therapeutics that could improve the feasibility of individualized, cell- and tissue-directed mRNA treatments.

Hickey JC, Roach T, Cassaidy B et al. · Molecular pharmaceutics · (2026) · View on PubMed ↗

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Neurodegeneration & neuroinflammation (AD/ALS/PD/FTD/DLB)

Microglial states revisited: from homeostasis to disease.

This review synthesized evidence on microglial state diversity across development, brain region, sex, age, genotype, and environment using advances such as single-cell/single-nucleus transcriptomics, chromatin accessibility profiling, and spatial multi-omics. It found that microglia occupy a multidimensional transcriptional state space that replaces binary “resting vs activated” or M1/M2 frameworks. Scientifically, this reframing improves how microglial “homeostatic” versus “disease-associated” programs are interpreted and targeted in neurodegenerative and other CNS disorders.

Eggen BJL, Kooistra SM · Nature reviews. Neuroscience · (2026) · View on PubMed ↗

Plasma proteome profiling identified biomarkers for the differential diagnosis and molecular staging of neurodegenerative dementias.

Large-scale plasma proteomics was used to profile 1,318 samples from international cohorts to identify blood biomarkers for differential diagnosis and molecular staging across Alzheimer’s disease (AD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD). More than 200 proteins were dysregulated across disease groups, with glial fibrillary acidic protein (GFAP) increasing along the AD continuum and integrin alpha-V and integrin alpha-M consistently reduced. This provides a scalable, blood-based molecular framework that could improve clinical stratification and staging of major neurodegenerative dementias.

Bellomo G, Vermunt L, In ‘t Veld S et al. · Nature aging · (2026) · View on PubMed ↗ · Free PDF ↗

Use of blood-based neurofilament light chain as an endpoint in clinical trials of neurodegenerative conditions: a scoping review.

This scoping review examined interventional neurodegenerative clinical trials (2013–2024) that used blood-based neurofilament light chain (serum or plasma NfL) as an endpoint. It found that blood NfL is increasingly used to quantify neuroaxonal injury and can serve as a trial endpoint, with variability in sampling matrices, assay approaches, and analytical frameworks. These insights are important for designing and standardizing future neurodegeneration trials using blood NfL to improve feasibility and comparability across studies.

Zheng Y, Bhalala OG, Chin KS et al. · Journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Multiomics integrative bioinformatics analysis of gene expression characteristics and molecular mechanisms in preeclampsia placental tissue.

This integrative multiomics bioinformatics analysis combined placental transcriptome and single-cell RNA-seq datasets from GEO to characterize gene expression features and molecular mechanisms in preeclampsia placental tissue. Using differential expression, Weighted Gene Co-expression Network Analysis (WGCNA), and machine-learning approaches, the study identified molecular subtypes and candidate pathways/genes associated with preeclampsia. The findings aim to improve mechanistic understanding and support biomarker or therapeutic target discovery for preeclampsia.

Li N, Tian L, Wei H · Artificial cells, nanomedicine, and biotechnology · (2026) · View on PubMed ↗ · Free PDF ↗

Mitochondria-targeted MXene-based nanozymes promote mitophagy and inhibit mtDNA-triggered cGAS/STING inflammation in osteoarthritis.

This preclinical study developed a mitochondria-targeted MXene-based nanozyme (MS@PMXene-TK with a mitochondria-targeting peptide MTP-131) to treat osteoarthritis and evaluated its effects on mitophagy and cGAS/STING inflammation. The key finding was that the nanozyme promoted mitophagy and inhibited mtDNA-triggered cGAS/STING inflammatory signaling, addressing mitochondrial dysfunction and chronic inflammation in OA models. These results suggest a subcellularly targeted therapeutic strategy that could improve cartilage repair by coupling ROS-responsive drug release with mitochondrial-directed immunomodulation.

Li T, Zheng A, Zhu C et al. · Bioactive materials · (2026) · View on PubMed ↗ · Free PDF ↗

Blood-based multimodal biomarker models for differentiating early-onset Alzheimer’s disease from frontotemporal dementia: a longitudinal study of early-onset dementia and family members (LEAF) study.

This longitudinal LEAF study evaluated blood-based multimodal biomarker models to differentiate early-onset Alzheimer’s disease (EOAD) from early-onset frontotemporal dementia (EOFTD) in patients aged ≤65 years, measuring plasma p-tau217, p-tau181, neurofilament light (NfL), and GFAP by immunoassay. The key finding was that plasma p-tau217 and p-tau181 showed high discriminative performance between EOAD and EOFTD (AUCs reported as 0.831 and 0.862, respectively). Clinically, these results support using plasma phospho-tau biomarkers—alone or in multimodal panels—to improve early-onset dementia diagnosis where evidence has been limited.

Kwon HS, Moon SY, Hwang M et al. · Journal of neurology · (2026) · View on PubMed ↗

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Neurobiology & CNS cell biology (mechanisms/structures)

Mechanism of actin thin filament pointed-end elongation by leiomodin.

This mechanistic study investigated how leiomodin (Lmod), particularly leiomodin-2 (Lmod2), promotes actin thin filament pointed-end elongation in striated muscle systems where actin exchange is biased toward the pointed end. The key finding was that leiomodin acts as an additional regulator of pointed-end actin filament growth, complementing known roles of capping proteins such as tropomodulin (Tmod) and CapZ and the molecular ruler nebulin. This advances understanding of how uniform thin-filament length is maintained in skeletal and cardiac muscle despite rapid turnover.

Brotzman SB, Palmer NJ, Boczkowska M et al. · Nature communications · (2026) · View on PubMed ↗

Mitochondrial-derived vesicles drive budding-type fission of damaged lysosomes.

The study identified a lysosomal renewal process called budding-type fission (B-fission) during hypoxia–reoxygenation stress and tested its mechanism in cells. It found that damaged lysosomes generate membrane buds that undergo scission to form small, functional lysosomes independently of autophagic lysosome reformation, with mitochondrial-derived vesicles (MDVs) delivering the fission adaptor MFF to lysosomes to recruit DRP1. This reveals a new, mitochondria-to-lysosome signaling route for maintaining lysosomal integrity under stress.

Luo Y, Yu J, Li Z et al. · Nature cell biology · (2026) · View on PubMed ↗

Promoter strength and position govern promoter competition through transcript-dependent insulation.

This study examined how promoter strength and genomic position determine promoter competition at the Sox2 locus by inserting diverse promoters into defined genomic sites and measuring effects on endogenous Sox2 transcription. It found that the reduction in endogenous Sox2 expression correlated with inserted promoter strength, that competition required transcription from the inserted promoter, and that longer transcripts produced more competition via transcript-dependent insulation. These results clarify the rules of promoter competition and provide mechanistic insight relevant to developmental gene regulation and disease-associated dysregulation.

Koska M, Nagano M, Swigut T et al. · Nature genetics · (2026) · View on PubMed ↗

The orchestration of ciliary opus: Interplay of signalling molecules, GTPases, and trafficking machinery.

This Current Opinion in Cell Biology review summarized how primary cilia signaling is orchestrated by the interplay of intraflagellar transport (IFT) machinery, the BBSome, small GTPases, and trafficking components. It emphasized that kinesin-2 and dynein-2 motors deliver receptors and signaling proteins into and out of cilia, while ciliary lipid composition and secondary messengers such as cAMP and Ca2+ regulate ciliary composition and signaling output. The synthesis highlights key mechanistic nodes that could be targeted to understand or treat ciliopathies and cilia-dependent disease.

Piyush R, Giri P, Shinde SR · Current opinion in cell biology · (2026) · View on PubMed ↗

Distribution of Big Tau Isoforms in the Human Central and Peripheral Nervous System.

This study used mass spectrometry to sequence and map “big tau” (tau isoforms containing exon 4a) across the human central and peripheral nervous system, including postmortem tissues from Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), and controls. It found distinct anatomical distributions of big tau isoforms between CNS and PNS regions and assessed their relative abundance in disease versus control samples. The results support big tau as a potentially disease-relevant biomarker/biological marker that extends tau research beyond canonical “small” tau isoforms.

Koppisetti RK, Barthélemy NR, Horie K et al. · Annals of neurology · (2026) · View on PubMed ↗

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Infectious disease virology & host-directed immunity

Circulating alpha-1 antitrypsin and its c-terminal peptides differentiate bacterial from viral community-acquired pneumonia.

In 81 prospectively enrolled adults with community-acquired pneumonia (CAP), the study tested whether circulating alpha-1 antitrypsin (AAT) and nine AAT-derived C-terminal peptides measured by ELISA and LC-based quantification could distinguish bacterial (n=36) from viral (n=45) CAP at admission and day 3. The key finding was that AAT and its C-terminal peptides provided discriminatory signal between bacterial and viral CAP. This could enable more accurate early etiologic diagnosis and reduce inappropriate antimicrobial use.

Pashai Fakhri M, Börner FR, Held J et al. · Journal of translational medicine · (2026) · View on PubMed ↗

Viral syncytia evolve to resist interferon.

The study examined how SARS-CoV-2 spike (S)-mediated syncytia formation affects antiviral interferon responses using cultured cells, human lung cell cultures, and hACE2 transgenic mice, including experiments with SARS-CoV-2 and SARS-CoV-2 S replacement vesicular stomatitis virus (VSV). It found that S-driven syncytia impair interferon antiviral effects and that spike substitutions modulating syncytia formation in Delta and Omicron similarly modulate interferon resistance, with additional effects on antibody-mediated neutralization. These results suggest syncytia are an evolutionary strategy for immune evasion, informing how viral entry/fusion phenotypes may influence treatment and vaccine effectiveness.

Li T, Kang I, Ye J et al. · Nature communications · (2026) · View on PubMed ↗

Mapping in-cell protein contact sites reveals hijacking of paraspeckles during influenza A virus infection.

In human cells infected with influenza A virus (IAV), the authors mapped native protein-protein contact sites using in-cell cross-linking mass spectrometry combined with structural modelling and functional assays. They uncovered previously unrecognized virus-host interactions, including host factors in the membrane-bound ER–Golgi system that regulate maturation of distinct haemagglutinin glycoforms, and progressive disassembly of paraspeckles during infection. This mechanistic map clarifies how IAV hijacks spatially organized host processes and identifies actionable host pathways for antiviral strategies.

Kotova I, Mühlberg L, Gilep K et al. · Nature microbiology · (2026) · View on PubMed ↗

All-trans retinoic acid suppresses systemic inflammation induced by severe fever with thrombocytopenia syndrome virus in mice.

The study examined whether all-trans retinoic acid (ATRA) modulates systemic inflammation during severe fever with thrombocytopenia syndrome virus (SFTSV) infection in patients and in an SFTSV mouse model. In patients, serum vitamin A/ATRA were depleted and correlated with worse systemic inflammatory response syndrome severity and mortality, while in mice intraperitoneal ATRA suppressed virus-induced hyperinflammation via PPARγ-mediated downregulation of macrophage AP-1 transcriptional activity. These results support ATRA as a potential host-directed anti-inflammatory therapy to reduce fatal inflammatory pathology in SFTSV.

Yu X, Wu J, Yin X et al. · Nature microbiology · (2026) · View on PubMed ↗

Viral protease-initiated lytic cell death as a universal antiviral mRNA therapy.

This Cell study developed viral protease-initiated lytic cell death (VID), a universal mRNA therapeutic platform by engineering gasdermin-D (GSDMD) with viral protease-specific cleavage motifs to trigger lytic cell death in virus-infected cells. Using hepatitis A virus (HAV) as a model, lipid nanoparticle (LNP)-encapsulated VIDA mRNA abolished viral replication and shedding in vivo and mitigated liver injury. The work suggests a broadly applicable mRNA strategy that converts viral protease activity into an intracellular “kill switch” for antiviral therapy.

Li L, Yan XL, Wang HY et al. · Cell · (2026) · View on PubMed ↗

Divergent Autophagy Pathways in Plasmodium: Mechanisms, Functions, and Therapeutic Potential.

This review studied autophagy in the malaria parasite Plasmodium, focusing on the reduced but functional autophagy-related (ATG) protein repertoire and the central role of ATG8. It found that Plasmodium ATG8 shows branched subcellular localization and associates with the apicoplast membrane, implying divergent autophagy pathway functions compared with yeast/mammals. These parasite-specific autophagy features highlight ATG8 and apicoplast-linked degradation as potential therapeutic targets for malaria.

Rajput S, Mehra P, Nandi R et al. · Molecular microbiology · (2026) · View on PubMed ↗

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Immunology & transplantation (T cells, innate immunity, complement)

EndoBridge 2025: pearls and highlights.

EndoBridge 2025 was a scientific meeting (Oct 23–26, 2025) that reviewed major topics in endocrinology and metabolism, including pituitary, thyroid, adrenal, bone metabolism, neuroendocrine tumors, diabetes, obesity, clinical nutrition, and lipid abnormalities. The key “finding” is that the congress delivered a comprehensive, state-of-the-art educational program with lectures and interactive case discussions covering current clinical and research directions across these areas. This is significant as a knowledge-update platform for clinicians and researchers, though it does not present new experimental results.

Yildiz BO, Armenti M, Brandi ML et al. · Hormones (Athens, Greece) · (2026) · View on PubMed ↗

Endothelial cell-intrinsic NOD2 signaling regulates the intestinal immune response through the generation of effector and memory T cells.

The authors investigated how endothelial cell-intrinsic NOD2 signaling regulates intestinal immunity by studying NOD2 engagement by muramyl dipeptide and its effects on T cell effector and memory generation. They found that NOD2 signaling in endothelial cells drives intestinal immune responses through T cell programming that supports both effector and memory T cell outcomes. This resolves part of the NOD2–Crohn’s disease paradox by linking NOD2 activation to adaptive immune homeostasis, informing therapeutic targeting of NOD2 pathways.

Tsankov BK, Denney M, Ahn JSY et al. · Nature immunology · (2026) · View on PubMed ↗ · Free PDF ↗

γδ T cells show distinct responses to CMV after stem cell transplantation.

This study examined how γδ T cells respond to cytomegalovirus (CMV) after allogeneic hematopoietic stem cell transplantation (aHSCT) by combining longitudinal single-cell RNA sequencing with paired T cell receptor (TCR) sequencing across five time points. It found patient-specific expansion of non-Vγ9Vδ2 γδ T cell clones, particularly within Vδ1+ and Vδ3+ subsets, associated with differences in CMV reactivation status. The work is significant because it provides clonal-resolution insight into immune reconstitution dynamics that could inform CMV monitoring and immunotherapeutic strategies post-transplant.

Sibbertsen F, Song Z, Ly C et al. · Journal of molecular medicine (Berlin, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

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Inflammation & autoimmune disease therapeutics

Caffeine and Cardiovascular Disease: A Scientific Statement From the American Heart Association.

This American Heart Association scientific statement reviewed evidence on caffeine intake and its associations with cardiovascular disease risk factors and cardiovascular outcomes across human observational studies and differing patterns of caffeine exposure. Overall findings suggest complex, heterogeneous effects with acute versus chronic differences and an inverse J-shaped relationship for naturally occurring caffeinated beverages in many studies. Clinically, the statement supports nuanced guidance that considers dose, beverage source, and individual susceptibility rather than a single universal cardiovascular effect of caffeine.

Marcus GM, Hu FB, van Dam RM et al. · Circulation · (2026) · View on PubMed ↗

Deucravacitinib in Active Psoriatic Arthritis: Efficacy and Safety up to 52 Weeks From the Randomized, Double-Blind, Phase 3 POETYK PsA-2 Trial.

The POETYK PsA-2 phase 3 randomized, double-blind trial assessed the efficacy and safety of deucravacitinib, an oral selective TYK2 inhibitor, in patients with active psoriatic arthritis who were biologic-naïve or previously treated with tumor necrosis factor inhibitors. Over 52 weeks, patients were randomized to deucravacitinib 6 mg daily, placebo, or apremilast 30 mg twice daily (safety reference), with primary efficacy based on ACR20 improvement at week 16 and continued treatment/switching thereafter. If efficacy and safety are confirmed through week 52, deucravacitinib could expand targeted oral options for PsA beyond TNF inhibitors and apremilast.

Mease PJ, Chandran V, Armstrong AW et al. · Arthritis & rheumatology (Hoboken, N.J.) · (2026) · View on PubMed ↗

Associations of viral infections and antiviral vaccinations with anti-NMDAR and other forms of autoimmune encephalitis.

This systematic literature review examined reported associations between viral infections and antiviral vaccinations and the occurrence of autoimmune encephalitis (AIE), including anti-NMDAR and other AIE subtypes. The key finding was that specific viral infection and vaccination links have been described across AIE subtypes, but the review highlighted gaps in a subtype-specific, frequency-based synthesis. Clinically, the work helps frame immunological triggers for AIE and underscores the need for more rigorous, quantifiable evidence to guide risk assessment around infections and antiviral vaccination.

Bamberg S, Schulte-Frankenfeld PM, Kreye J · Brain, behavior, & immunity - health · (2026) · View on PubMed ↗ · Free PDF ↗

Eltrombopag Added to Standard Immunosuppressive Treatment as Front-Line Therapy for Severe Aplastic Anemia: Long-Term Outcomes of the Phase-3 Randomized Superiority EBMT-SAAWP RACE Study.

This phase 3 randomized superiority trial (EBMT-SAAWP RACE; NCT02009747) studied whether adding eltrombopag to standard immunosuppressive therapy (horse ATG plus cyclosporine A) improves long-term outcomes in treatment-naïve severe aplastic anemia. The key finding from the final 2-year analysis was that eltrombopag plus standard IST produced a significantly higher 2-year cumulative incidence of complete response than standard IST alone (reported as 62.4% vs the comparator arm). This provides longer-term evidence that eltrombopag can enhance first-line response rates in severe aplastic anemia, potentially improving durability of treatment outcomes.

Risitano AM, Iacobelli S, Kulasekararaj A et al. · American journal of hematology · (2026) · View on PubMed ↗ · Free PDF ↗

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Respiratory disease (asthma/COPD/ARDS/RSV/influenza)

Phase III LUNA clinical programme: design of four randomised, double-blind, placebo-controlled studies assessing the efficacy and safety of tozorakimab in patients with symptomatic COPD and a high risk of exacerbations.

The LUNA programme was designed as four multicentre, randomized, double-blind, placebo-controlled phase III studies to test tozorakimab (anti-IL-33 monoclonal antibody) in symptomatic COPD patients with a high risk of exacerbations despite optimized inhaled therapy. The trials evaluate efficacy and safety across OBERON (NCT05166889) and TITANIA (NCT05158387) and two additional ongoing studies, targeting both IL-33 reduced (IL-33red) and oxidised (IL-33ox) activity. This programme aims to determine whether IL-33 blockade improves exacerbation outcomes and disease control in a high-risk COPD population.

Watz H, Sciurba FC, Bonini M et al. · BMJ open respiratory research · (2026) · View on PubMed ↗

Use of tezepelumab for chronic rhinosinusitis with nasal polyps by eosinophilic endotype: WAYPOINT post-hoc analysis.

This WAYPOINT post-hoc analysis evaluated tezepelumab 210 mg versus placebo every 4 weeks in Japanese adults with severe chronic rhinosinusitis with nasal polyps (CRSwNP), stratified by eosinophilic chronic rhinosinusitis defined by the Japanese Epidemiological Survey of Refractory Eosinophilic Chronic Rhinosinusitis (ECRS) endotype. Tezepelumab improved nasal polyp outcomes (including total Nasal Polyp Score) and sinonasal symptoms and showed a consistent safety profile across the eosinophilic subgroups, with reduced need for surgery and systemic corticosteroids reported in the parent trial. The results support tezepelumab as an endotype-relevant biologic option for CRSwNP in Japanese clinical practice, potentially reducing steroid exposure and surgical burden.

Fujieda S, Otori N, Han JK et al. · Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · (2026) · View on PubMed ↗

Effect of high-dose versus standard-dose influenza vaccines on hospitalisation outcomes and mortality in older adults: a systematic review and meta-analysis.

This systematic review and meta-analysis compared high-dose inactivated influenza vaccine (HD-IIV; 60 μg haemagglutinin per strain) versus standard-dose inactivated influenza vaccine (SD-IIV) in adults aged 65 years or older using randomized controlled trials. It found that HD-IIV provides improved protection against clinically important outcomes, including influenza-related hospitalization and mortality, relative to SD-IIV in older adults. The findings support preferential use of HD-IIV in geriatric immunization strategies to reduce severe influenza burden.

Zhao W, Lian R, Zhao Y et al. · The lancet. Healthy longevity · (2027) · View on PubMed ↗

Clesrovimab in Infants at Increased Risk For Severe Disease During 2 RSV Seasons: A Randomized Clinical Trial.

This randomized clinical trial evaluated clesrovimab, a long-acting monoclonal antibody, in infants at increased risk for severe respiratory syncytial virus (RSV) disease across two RSV seasons, comparing clesrovimab (105 mg) with palivizumab in season 1 and assessing safety/tolerability of 210 mg clesrovimab in season 2. The key finding was that clesrovimab was safe and tolerable in this high-risk infant population across the two seasons, with pharmacokinetic characterization reported for the second-season dosing. Clinically, it provides evidence supporting continued prophylaxis with clesrovimab for infants who remain at high risk for severe RSV beyond the first season.

Zar HJ, Bont LJ, Manzoni P et al. · JAMA pediatrics · (2026) · View on PubMed ↗

Prone positioning in ARDS.

This article reviewed the evidence and clinical role of prone positioning in acute respiratory distress syndrome (ARDS), including early use in intubated patients with PaO2/FiO2 <150 mmHg and the awake prone position (APP) in non-intubated patients. The key finding is that prone positioning consistently improves oxygenation and has evolved from rescue therapy to an integral lung-protective ventilation strategy, with expanded application during and after COVID-19. This is clinically significant because it supports routine incorporation of prone strategies to improve respiratory outcomes while clarifying where confirmation is still needed for broader non-COVID ICU practice.

Ehrmann S, Li J, Liu L et al. · Intensive care medicine · (2026) · View on PubMed ↗ · Free PDF ↗

The Airway Transcriptome in Type 2 Cytokine Biomarker-High and -Low Severe Asthma.

This study analyzed airway transcriptomic profiles from bronchial biopsies and brushes to compare molecular pathways in severe asthma patients with type 2 (T2) cytokine biomarker-high versus biomarker-low states. Using data from the UK Refractory Asthma Stratification Programme cohort (18 T2-high, 23 T2-intermediate, 11 T2-low) plus 20 healthy controls, and assessing samples pre- and post-treatment with high-dose inhaled corticosteroids, the authors identified dysregulated genes and pathways distinguishing T2 biomarker strata. The work supports transcriptome-informed stratification of severe asthma and may help identify biomarkers and targeted therapies for T2-low disease where mechanisms remain unclear.

Shen J, Chaudhuri R, Bicknell S et al. · Allergy · (2026) · View on PubMed ↗ · Free PDF ↗

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Cardiovascular & metabolic disease (diabetes/obesity/heart failure/CV risk)

Does Characterization of Phenotypic Heterogeneity Provide Mechanistic Insights or Influence the Response to Treatment? Experience in Positive and Neutral Trials in Patients With Heart Failure and a Preserved Ejection Fraction.

This article reviewed and analyzed whether characterizing phenotypic heterogeneity in heart failure with preserved ejection fraction (HFpEF) can yield mechanistic insights or identify treatment responders, drawing on experience from positive and neutral HFpEF trials. The key finding was that despite extensive subgrouping efforts, phenotypic heterogeneity characterization has not reliably identified responders or translated into broadly effective, mechanism-driven therapies. Clinically, it highlights the need for better causal frameworks and trial designs beyond descriptive phenotyping to guide HFpEF treatment selection.

Packer M, Schiattarella GG, Petrie MC et al. · Circulation · (2026) · View on PubMed ↗

Loss of ATP-Dependent Citrate Lyase Drives Left Ventricular Dysfunction by Metabolic Remodeling.

This study examined how loss of ATP-dependent citrate lyase (ACLY/Acly) affects cardiac metabolism and function by using human heart tissue from healthy donors and patients with nonischemic cardiomyopathy and applying CRISPR-based approaches to model ACLY loss. The key finding was that ACLY loss drives left ventricular dysfunction through metabolic remodeling, consistent with impaired acetyl-CoA production and downstream lipid synthesis programs. Scientifically, it identifies ACLY as a metabolic regulator of cardiac adaptation and suggests that metabolic pathway modulation could be a therapeutic strategy in nonischemic cardiomyopathy.

Liu S, Gammon ST, Tan L et al. · Circulation · (2026) · View on PubMed ↗

Implications of the 2026 Dyslipidemia Guideline for Primary Prevention Statin Therapy.

This study assessed the population health impact of the 2026 American Heart Association/American College of Cardiology/multisociety dyslipidemia guideline on primary prevention statin eligibility among nonpregnant adults aged 30–79 years without known ASCVD in NHANES 2017–2023. The guideline’s updated ASCVD risk estimation and expanded statin-eligible populations were projected to change the proportion of adults recommended for statin therapy. These findings are clinically significant for anticipating downstream effects on preventive cardiovascular care delivery and population-level ASCVD risk reduction.

Anderson TS, Wilson LM, Sussman JB · JAMA · (2026) · View on PubMed ↗

Effects of Lifestyle Modification on Intrapancreatic Fat Deposition: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis evaluated whether lifestyle modification reduces intrapancreatic fat deposition (IPFD) in humans, synthesizing evidence from PubMed and Embase studies. Across included studies, lifestyle interventions showed beneficial effects on IPFD, supporting IPFD as a modifiable ectopic fat depot linked to pancreatic disease risk. The results are scientifically and clinically relevant because they strengthen the rationale for lifestyle-based strategies to target pancreatic fat accumulation and potentially lower future endocrine/exocrine pancreatic morbidity.

Ahmad S, Sul HH, Danpanichkul P et al. · Current obesity reports · (2026) · View on PubMed ↗ · Free PDF ↗

GLP-1 Receptor Agonists and All-Cause Overdose Risk in Veterans With Type 2 Diabetes and Opioid Use Disorder.

This target trial emulation study used Veterans Health Administration data to assess all-cause overdose risk among Veterans with type 2 diabetes and opioid use disorder who initiated semaglutide or tirzepatide versus comparison diabetes medications. The key finding was that GLP-1 receptor agonist initiation was associated with a different (replicated) overdose risk profile compared with non-GLP-1 diabetes treatments. This is clinically significant because it informs risk-benefit considerations for GLP-1RA use in a high-risk population with OUD.

Kennedy KP, Bremseth-Vining R, Lynch KG et al. · The Journal of clinical psychiatry · (2026) · View on PubMed ↗

Small Extracellular Vesicles From Cardiomyocytes Activate Microglia Aggravating HFpEF.

The study investigated whether small extracellular vesicles (sEVs) released from cardiomyocytes activate hypothalamic microglia and worsen HFpEF in a mouse model combining a long-term high-fat diet with the nitric oxide synthase inhibitor L-NAME. sEV-driven microglial activation and hypothalamic inflammation were observed, and microglial depletion using the CSF1R inhibitor PLX3397 suppressed downstream sympathetic activation. These results implicate a heart-to-brain sEV–microglia pathway as a mechanistic driver of HFpEF neuroinflammation and suggest microglial targeting as a potential therapeutic strategy.

Men L, Wang Q, Ren B et al. · Circulation research · (2026) · View on PubMed ↗

Durability and Safety of Imeglimin as an Add-On to DPP-4 Inhibitors in Japanese Type 2 Diabetes: The 104-Week FAMILIAR Trial.

This multicenter randomized placebo-controlled trial evaluated imeglimin as an add-on to DPP-4 inhibitors in Japanese adults with type 2 diabetes, including a focus on glycemic durability and safety over 104 weeks (FAMILIAR; 24-week double-blind followed by 80-week open-label extension). The key finding was that imeglimin added to existing DPP-4 inhibitor therapy produced sustained HbA1c improvements through week 104 with an acceptable safety profile, including in elderly patients. These results support long-term imeglimin combination therapy as a durable and tolerable intensification option for Japanese patients inadequately controlled on DPP-4 inhibitors.

Shimoda M, Osonoi T, Iwamoto M et al. · Diabetes, obesity & metabolism · (2026) · View on PubMed ↗

Peptide LKLKLL is a more effective component of Akkermansia muciniphila which regulate glucolipid metabolism through GLP-1/GIP dual modulation.

This preclinical study examined the metabolic effects of the Akkermansia muciniphila–derived hexapeptide LKLKLL on glucolipid metabolism and incretin signaling in cell models and mouse models of obesity/diabetes. It found that LKLKLL improved glucose tolerance and reduced body weight in high-fat diet–induced obese mice while enhancing GLP-1 secretion and modulating GLP-1/GIP dual pathways. These findings suggest LKLKLL as a defined, translational alternative to live A. muciniphila for metabolic disease interventions targeting GLP-1/GIP signaling.

Li Y, Ye D, Fu C et al. · Gut microbes · (2026) · View on PubMed ↗ · Free PDF ↗

Work-to-sleep ratio as a novel marker of NAFLD risk: evidence from U.S. and Korean national cohorts.

This cohort study assessed whether the work-to-sleep ratio (WSR) predicts risk of NAFLD/MASLD using U.S. and Korean national cohorts. The key finding is that WSR, which integrates occupational time and sleep recovery into a single behavioral metric, is associated with NAFLD risk beyond work hours or sleep duration alone. Clinically, WSR could serve as a practical risk marker to identify individuals who may benefit from sleep- and workload-targeted interventions.

Zhong Y, Kou Y, Lu Z et al. · Nutrition & metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

Activity-based proteomics analysis revealed that DNJ directly targeted ATP5F1 to alleviate high glucose induced cardiomyocyte injury.

This study examined the cardioprotective mechanism of the natural alkaloid 1-deoxynojirimycin (DNJ) in cardiomyocytes exposed to high glucose, using activity-based protein profiling (ABPP) to identify DNJ direct targets and mechanistic assays to define downstream effects. The key finding was that DNJ directly targeted ATP5F1 (a mitochondrial ATP synthase subunit) and that this interaction alleviated high-glucose-induced cardiomyocyte injury. Scientifically, it provides a direct molecular target for DNJ in diabetic cardiomyopathy and implicates mitochondrial ATP synthase dysfunction as a therapeutic vulnerability.

Li X, Chen Y, Yang H et al. · Cell communication and signaling : CCS · (2026) · View on PubMed ↗ · Free PDF ↗

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Musculoskeletal & rehabilitation (sarcopenia/arthritis/pain)

The 2026 British Society for Rheumatology guideline for pain management in people with inflammatory arthritis.

This article reports the 2026 British Society for Rheumatology guideline for pain management in people with inflammatory arthritis (IA), synthesizing evidence from trial data, electronic health record analyses, and patient survey findings. It addresses the observed mismatch between real-world long-term opioid/gabapentinoid prescribing and the lack of trial evidence for efficacy, and emphasizes underused non-pharmacological pain care with supportive evidence. The guideline provides an evidence-based, UK-specific framework to improve pain outcomes and reduce reliance on ineffective long-term pharmacotherapies in IA.

Scott IC, Smith TM, Babatunde O et al. · Rheumatology (Oxford, England) · (2026) · View on PubMed ↗

Immune-Enhancing Nutrition and Outcomes After Radical Cystectomy: A Randomized Clinical Trial.

This multicenter, randomized, double-blind phase 3 clinical trial (SWOG S1600) studied whether perioperative specialized immunonutrition reduces 30-day complications compared with standard oral nutrition support in adults undergoing radical cystectomy for bladder cancer. The key finding was that immune-enhancing immunonutrition improved perioperative outcomes by reducing complications within 30 days relative to standard nutrition. Clinically, it supports using targeted perioperative nutritional formulations as an adjunct strategy to improve surgical safety in radical cystectomy patients.

Hamilton-Reeves JM, Unger JM, Holzbeierlein JM et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

Unlocking Sulforaphane’s Potential in Friedreich Ataxia: Further Evidence from Preclinical Investigations Using Induced Pluripotent Stem Cell-Derived Sensory Neurons.

This preclinical study tested sulforaphane (SF) against omaveloxolone (Omav) and dimethyl fumarate (DMF) in induced pluripotent stem cell (iPSC)-derived sensory neurons from Friedreich ataxia patients with expanded GAA repeats in the FXN gene (e.g., 550 GAA1 repeats). The key finding was that SF further supported FXN expression and modulated oxidative stress and inflammatory pathways in these patient-derived neurons, extending prior evidence for SF’s therapeutic potential. This is significant because it provides additional preclinical support for SF as a candidate therapy alongside the only approved treatment, omaveloxolone, for FRDA.

Yang W, Thompson B, Miellet S et al. · Antioxidants & redox signaling · (2026) · View on PubMed ↗

PROSPECT guideline for total hip arthroplasty: updated systematic review and procedure-specific postoperative pain management recommendations.

This PROSPECT guideline update performed a systematic review to revise procedure-specific postoperative pain management recommendations for elective primary total hip arthroplasty. It focused on randomized controlled trials and systematic reviews published between January 2020 and June 2024 evaluating peri-operative analgesic or surgical interventions, with emphasis on newer evidence including motor-sparing regional techniques. The guideline is intended to standardize evidence-based pain control strategies after total hip arthroplasty to improve recovery while balancing efficacy and safety.

Carella M, Bugada D, Van de Velde M et al. · Anaesthesia · (2026) · View on PubMed ↗

Targeting BLyS and APRIL with Telitacicept versus Conventional Immunotherapy in Generalized Myasthenia Gravis: A Comparative Study.

This retrospective real-world comparative study evaluated telitacicept versus conventional immunotherapy in patients with acetylcholine receptor antibody-positive generalized myasthenia gravis (AChR-Ab+ gMG), using propensity score matching (1:1) in a broader population than prior trials. The key finding was that telitacicept showed differences in treatment response and safety outcomes relative to conventional immunotherapy after matching (35 patients per group). Clinically, the study supports telitacicept’s effectiveness and tolerability in routine practice for AChR-Ab+ gMG beyond the narrower populations of earlier randomized evidence.

Yang Y, Kang N, Zhu Y et al. · ImmunoTargets and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Electroacupuncture Treatment on Sarcopenia in Patients Undergoing Maintenance Haemodialysis: An Effective Therapy.

This randomized controlled clinical study evaluated electroacupuncture (EA) as a treatment for sarcopenia in patients undergoing maintenance haemodialysis (MHD), comparing 36 participants assigned to EA versus control. It found that EA delivered over 24 sessions (30 minutes, three times weekly) improved sarcopenia outcomes compared with continuing usual care. Clinically, EA may represent a non-pharmacologic adjunct to improve muscle health in MHD patients with sarcopenia.

Chen R, Qian Q, Wang B et al. · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗ · Free PDF ↗

Efficacy of magnesium-calcium ionic oral rinse for primary burning mouth syndrome: a randomized, double-blind, placebo-controlled trial.

This randomized, double-blind, placebo-controlled trial studied the efficacy and safety of a magnesium–calcium ionic oral rinse in patients with primary burning mouth syndrome (BMS). The key finding was that the magnesium–calcium oral rinse improved outcomes compared with placebo (with efficacy and safety assessed across trial endpoints). This supports a local, ionic microenvironment–modulating strategy as a potentially safer alternative to systemic therapies for chronic orofacial neuropathic pain.

Carrió N, Garawani BE, Alahmad A et al. · BMC oral health · (2026) · View on PubMed ↗ · Free PDF ↗

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Methods, guidelines & population health (epidemiology, trials, biomarkers, devices)

Genome-wide association analyses of borderline personality disorder identify 11 loci and highlight shared risk with mental and somatic disorders.

A genome-wide association study meta-analysis of borderline personality disorder (BPD) was conducted in European-ancestry samples (12,339 cases/1,041,717 controls discovery; 685 cases/107,750 controls replication). The study identified 11 independent risk loci and 9 risk genes, with SNP-heritability of 17.3% and polygenic scores explaining 4.6% of BPD liability-scale variance. These findings refine the genetic architecture of BPD and highlight shared genetic risk with mental and somatic disorders, supporting cross-diagnostic biology for future mechanistic work and risk prediction.

Streit F, Awasthi S, Hall ASM et al. · Nature genetics · (2026) · View on PubMed ↗

COVID-19 and Global Perinatal Health: Lessons Learned on Maternal-Neonatal Outcomes, Infant Feeding Practices, and Healthcare Economics Across Income Settings.

This narrative review synthesized evidence on how the COVID-19 pandemic affected maternal-neonatal outcomes, infant feeding practices, and healthcare economics across high-income countries (HICs) and low- and middle-income countries (LMICs). It found that both direct SARS-CoV-2 infection and indirect healthcare-system disruption were associated with worse perinatal outcomes, altered breastfeeding practices, and substantial financial burden on healthcare institutions, with larger impacts in resource-limited settings. These cross-setting findings highlight where maternal-newborn care and breastfeeding support need strengthening during ongoing or future respiratory pandemics.

Gunasekaran V, Woo S, Shetty AK et al. · American journal of perinatology · (2026) · View on PubMed ↗

Global, regional, and national burden of road injuries 1990-2023: a systematic analysis for the Global Burden of Disease Study 2023.

This Global Burden of Disease Study 2023 analysis estimated incidence, mortality, and morbidity of road injuries across 204 countries and territories from 1990 to 2023 by road injury type and nature-of-injury categories. It quantified the global and regional trends in road injury burden and identified where progress toward road-safety targets remains insufficient. These estimates provide an evidence base for targeting interventions to reduce road traffic deaths and serious injuries by 2030.

The Lancet. Public health · (2026) · View on PubMed ↗

Structures of dynamic interactors at native proteasomes by PhIX-MS and cryo-electron microscopy.

This Molecular Cell study introduced PhIX-MS (photo-induced in situ crosslinking-mass spectrometry) combined with cryo-electron microscopy to capture dynamic, transient interactors at native proteasomes. Applying the workflow, the authors mapped the redox sensor TXNL1 at the proteasome regulatory particle (RP), including its dynamic thioredoxin-like domain near RPN2/PSMD1 and RPN13/ADRM1, and resolved RP structures bound to TXNL1. The approach clarifies how redox sensing is physically coupled to proteasome regulation and substrate processing.

Lee K, Negi H, Chen X et al. · Molecular cell · (2026) · View on PubMed ↗

Multidomain Lifestyle Intervention in Mild Cognitive Impairment: Subgroup Analysis of the SUPERBRAIN-MEET Randomized Trial.

This prespecified subgroup analysis of the 24-week SUPERBRAIN-MEET randomized controlled trial studied whether a multidomain lifestyle intervention (MLI) delivered via face-to-face sessions plus digital platforms improved cognition differently by sociodemographic factors, digital readiness, baseline cognitive status, and vascular risk in people with mild cognitive impairment (MCI). The key finding was that the cognitive benefits of the MLI varied across these baseline subgroup characteristics rather than being uniform across all participants. Clinically, this suggests that tailoring multidomain lifestyle programs to patients’ baseline cognitive status, digital readiness, and vascular risk may improve dementia-prevention effectiveness in MCI.

Kim DA, Lee SM, Sun K et al. · Neurology · (2026) · View on PubMed ↗

A genome-wide functional analysis of conserved intronic regions reveals essential roles for speckle-associated retained introns.

This genome-wide functional study used a dual CRISPR-Cas editing strategy to delete 2,600 conserved human intronic regions and tested their roles in cell fitness, focusing on speckle-associated retained introns. The key finding was that a subset of these conserved “fitness” intronic sequences affects cell growth by altering intron retention and host gene expression, including speckle-associated retained introns in FNBP4 and DDX5 that produced downstream effects. Scientifically, it establishes that conserved retained introns in nuclear speckles are functionally essential regulatory elements rather than nonfunctional sequence remnants.

Farhangmehr S, Braunschweig U, Wu M et al. · Cell reports · (2026) · View on PubMed ↗

Accelerated Epigenetic and Inflammatory Aging and Intrinsic Capacity.

This population-based cohort study investigated cross-sectional and longitudinal associations between accelerated epigenetic aging and accelerated inflammatory aging with intrinsic capacity (IC), a WHO-defined composite of physical and mental capacities, and examined sex differences and interactions. The key finding was that accelerated epigenetic and inflammatory aging were associated with lower IC and that these aging measures showed domain-specific and interactive relationships with IC decline over time. Scientifically and clinically, it supports using molecular aging biomarkers to identify individuals at risk for reduced functional capacity and to guide preventive interventions for healthy longevity.

Rouch L, De Souto Barreto P, Rolland Y et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

Gut Metabolism Links Precision Nutrition, Exercise, and Healthspan in Drosophila melanogaster.

This Drosophila melanogaster study used a chemically defined diet to test whether a multimodal longevity intervention—methionine restriction (MR), taurine supplementation (Tau), and moderate exercise—extends lifespan without impairing physiological performance. The combination additively increased lifespan while preserving reproductive capacity and improving locomotor function, and targeted metabolomics with stable isotope tracing indicated increased mitochondrial TCA cycle flux and improved gut redox homeostasis. Scientifically, it supports a gut-metabolism-centered model for coordinating healthspan and longevity benefits from dietary and exercise interventions.

Wei F, Liu S, Sun Y et al. · Aging cell · (2026) · View on PubMed ↗ · Free PDF ↗

Medical Students’ Attitudes, Perceptions, and Self-Reported Familiarity With Artificial Intelligence in Healthcare: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis synthesized studies reporting medical students’ attitudes, perceptions, and self-reported familiarity with artificial intelligence in healthcare. It focused on harmonizing constructs across heterogeneous survey instruments and quantified variation and heterogeneity across settings using meta-analytic methods. The results provide an evidence base for designing AI literacy and education interventions tailored to students’ baseline familiarity and attitudes.

Zhang W, Han J, Han X et al. · JMIR medical education · (2026) · View on PubMed ↗ · Free PDF ↗

Ruxolitinib cream in adults with moderate atopic dermatitis after failure of other topicals: A randomized trial.

This randomized trial studied ruxolitinib cream in adults (≥18 years) with moderate atopic dermatitis (IGA 3, EASI >7, itch NRS ≥4) who had inadequate response, intolerance, or contraindications to topical corticosteroids (TCS) and topical calcineurin inhibitors (TCI) in the prior 12 months (TRuE-AD4; NCT06238817). The 8-week results reported that ruxolitinib cream improved disease signs/symptoms compared with the trial comparator in this post–TCS/TCI population. These findings support ruxolitinib cream as a targeted topical option for moderate atopic dermatitis when standard topical therapies fail.

Carrascosa JM, Prajapati VH, Hong HC et al. · Journal of the European Academy of Dermatology and Venereology : JEADV · (2026) · View on PubMed ↗ · Free PDF ↗

Evaluating the pharmacokinetics, efficacy and safety of low-dose cannabidiol.

This review studied pharmacokinetics (PK), pharmacodynamics (PD), and safety of low-dose cannabidiol (CBD) at doses ≤2.5 mg/kg or ≤175 mg/day, focusing on oral CBD PK studies ≤150 mg. It found that low-dose CBD produces substantially lower systemic exposure (Cmax and AUC) than typical Epidiolex dosing and showed very limited evidence of physical or neurological PD effects in healthy volunteers. The review is significant for interpreting real-world low-dose CBD use and for guiding evidence-based dosing and safety expectations.

Warren WG, Osborn M, Yates A et al. · British journal of clinical pharmacology · (2026) · View on PubMed ↗

Frailty mediates the association between sleep duration and physical, psychological, and cognitive multimorbidity in Chinese middle-aged and older adults.

This study analyzed whether frailty mediates the association between sleep duration and physical, psychological, and cognitive multimorbidity (PPC-MM) in Chinese middle-aged and older adults using CHARLS data (cross-sectional n=7,193; longitudinal n=5,380). It found nonlinear relationships between sleep duration and PPC-MM risk and that frailty partially mediated this association in both cross-sectional and longitudinal models. These findings suggest that targeting frailty could be a practical intervention pathway linking sleep health to multimorbidity risk.

Ding H, Li L, Luo G et al. · Scientific reports · (2026) · View on PubMed ↗ · Free PDF ↗

Sustainable miniaturized smartphone-coupled TLC platform for innovative cleaning validation: application to tizanidine combinations under challenging concentration ratios.

This analytical methods study developed a sustainable, miniaturized smartphone-coupled thin-layer chromatography (TLC) platform to validate cleaning for pharmaceutical manufacturing of tizanidine (TZN) combinations with aceclofenac (ACF), ibuprofen (IBF), and paracetamol (PRC). The key finding is that the at-line portable TLC approach enables determination of TZN under challenging concentration ratios while addressing cross-contamination risk for a narrow therapeutic index, high-abuse-potential drug. Clinically and operationally, the platform offers a rapid, field-deployable tool to improve routine cleaning validation and reduce patient-safety risks from carryover.

Abd El-Aziz MO, Nadim AH, Monir HH et al. · Scientific reports · (2026) · View on PubMed ↗ · Free PDF ↗

Gut microbiota-driven metabolites modulate the development of stress-related mental disorders.

This review synthesized evidence from preclinical and clinical studies on how gut microbiota-driven metabolites influence the development of stress-related mental disorders such as depression, anxiety, and post-traumatic stress disorder. The key finding is that microbiota alterations change the production of circulating metabolites that modulate host physiology and thereby contribute to stress-disorder pathophysiology. Scientifically, it frames metabolite-mediated gut–brain mechanisms as actionable targets for future therapeutic strategies.

Yuan M, Qin F, Wu L et al. · Translational psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗

Sodium bicarbonate therapy in severe metabolic acidemia: an individual patient data meta-analysis of the BICAR-ICU and BICAR-ICU2 trials.

This individual patient data meta-analysis combined the BICAR-ICU and BICAR-ICU2 randomized trials to assess intravenous sodium bicarbonate therapy in adults with severe metabolic acidemia (pH ≤ 7.20), comparing bicarbonate titrated to pH ≥ 7.30 versus no bicarbonate. The key finding is the pooled effect on 90-day mortality and renal replacement therapy (RRT) use, including evaluation of heterogeneity across prespecified subgroups. The clinical significance is that it clarifies whether sodium bicarbonate provides outcome and kidney-protection benefits in severe acidemia and for which patient groups.

Fosset M, Pensier J, Jabaudon M et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Lyophilized platelet derived extracellular vesicles promote hemostasis and attenuate intracranial hemorrhage following traumatic brain injury.

This study evaluated whether lyophilized platelet-derived extracellular vesicles (LPEVs) reduce intracranial hemorrhage (ICH) and preserve blood–brain barrier (BBB) integrity after traumatic brain injury (TBI) using characterization by flow cytometry, scanning electron microscopy, and Nanosight plus in vitro human brain endothelial barrier assays and a murine TBI model. The key finding was that LPEVs promoted hemostasis and attenuated ICH while maintaining BBB integrity following TBI. Clinically, this supports LPEVs as a potentially translatable, off-the-shelf biologic approach to limit hemorrhagic complications after TBI.

Trivedi A, Miyazawa B, Fields AT et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Generated automatically on July 22, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.