Table of Contents Alert: The FASEB Journal, Vol. 39, No. 22, 30 November 2025
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The FASEB Journal Volume 39, Issue 22 30 November 2025 |
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REVIEW ARTICLE
Open AccessRecent Advancements in the Research of the Mechanism by Which PPAR‐γ Is Involved in Postoperative Neurocognitive Disorder
e71243 | First Published: 17 November 2025
PPAR-γ plays a crucial role in the pathogenic mechanisms and regulation of PND. Its pathways are intricately intertwined with inflammatory responses, oxidative stress, β-amyloid deposition, and abnormal phosphorylation of Tau protein.
RESEARCH ARTICLE
Glycosylation of Tetraspanin CD151 Defines the Invasive Phenotype of Human Breast Cancer Cells
e71236 | First Published: 11 November 2025
Integrated N-glycosylation status of CD151 contributes to invasive activity in breast cancer cells. There are mainly three types of N-glycosylation status in CD151: oligomannose-type, complex-type, and no-glycosylation. The oligomannose-type glycan inhibits the association with integrin α3, while the complex-type glycan and the no-glycosylation form do not inhibit the association with integrin α3. The invasive activity of the breast cancer cells is integrated in these states. Non-glycosylated forms exhibit strong invasion activity that defines the invasive phenotype of breast cancer patients.
Biochemical Modifications of Homocysteine Drive Neutrophil Extracellular Trap Formation in Ischemic Stroke
e71221 | First Published: 13 November 2025
Peripheral neutrophils upon stimulation with homocysteine and its modifications induce NETosis and DNA damage in an ERK/AKT/PAD4-dependent signaling pathway. Hyperhomocysteine mouse models exhibit elevated NETs markers, platelet activation, reduced motor function, and neuronal damage, and administration of anti-NETs agents reverses the deteriorative effects. Stroke subjects display elevated homocysteine, NETs components, and autoantibodies against homocysteinylated serum albumin.
FOXM1 Facilitates NSCLC Tumorigenesis Through the Transcriptional Regulation of UBE2C
e71230 | First Published: 12 November 2025
FOXM1, a key transcriptional driver, and UBE2C, a mitotic regulator, are co-overexpressed in NSCLC. FOXM1 transcriptionally activates UBE2C, promoting tumor proliferation, invasion, and progression. FAM64A enhances FOXM1 stability, further amplifying oncogenic signaling. Targeting the FAM64A/FOXM1/UBE2C axis suppresses tumor growth, revealing a critical pathway and promising therapeutic target in NSCLC.
Open AccessKynurenine Pathway Dysregulation Impairs Podocyte Morphology and Bioenergetics In Vitro and Leads to Glomerular Dysfunction
e71228 | First Published: 12 November 2025
The enzymes of the kynurenine pathway participate in the catabolism of TRP, where they generate metabolites known as kynurenines, which are considered biologically active. Using a transgenic zebrafish line, we showed that systemic changes in the kynurenine pathway lead to edema and proteinuria, both signs of an impaired glomerular filtration barrier. Additionally, inhibition of the pathway in cultured podocytes resulted in alterations to the cytoskeleton, increased cell detachment, and changes in redox status and mitochondrial function.
Open AccessEye‐Targeted A20 Gene Therapy Alleviates Ischemic Retinopathy by Reducing Pathologic Neovascularization, Gliosis, and Neuronal Apoptosis
e71226 | First Published: 12 November 2025
Eye-targeted A20 gene therapy alleviates ischemic retinopathy by limiting pathologic neovascularization, reducing gliosis, and protecting from neuronal apoptosis.
ADAM8 Destroys the Endothelial Barrier and Promotes Leukocyte Extravasation to Aggravate Hepatic Ischemia–Reperfusion Injury
e71217 | First Published: 12 November 2025
Hepatic ischemia–reperfusion injury (HIRI) is a local aseptic inflammatory response driven by innate immunity, and it can severely damage liver function. In this work, we found that ADAM8 expression was increased in the liver tissues of HIRI mice, which was also correlated with the progression of liver damage. Suppression of ADAM8 abated HIRI development by disrupting the endothelial barrier, increasing endothelial permeability, accelerating leukocyte extravasation, and the inflammatory response.
Open AccessLipoxin A4 Regulates M2 Macrophage‐Derived Exosomal miR‐25‐5p to Protect Cell Pyroptosis in Bronchopulmonary Dysplasia
e71218 | First Published: 12 November 2025
In premature infants with BPD treated with LXA4, circulating monocytes are reprogrammed and polarized into M2-Mφs and then migrate into the lungs. The M2-exo released by M2-Mφs, which is rich in miR-25-5p, downregulates the PI3K/AKT signaling pathway by acting on the target gene NRBP2, thereby inhibiting the pyroptosis of AT2. The secretion of GSDMD-N and inflammatory factors from the latter is reduced, alleviating the destruction of AT2 and inflammatory responses, and improving BPD-induced lung injury.
HMGB2 Deficiency in Bone Marrow Mesenchymal Stem Cells Promotes Age‐Related Osteoporosis by Inhibiting Osteoblast Differentiation via Inflammatory Factors
e71235 | First Published: 13 November 2025
High mobility group box 2 (HMGB2) is essential in osteoporosis patients and can be used to treat osteoporosis by promoting osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). HMGB2 knockdown in senescent BMSCs inhibited osteogenic differentiation, and overexpression of HMGB2 promoted osteogenic differentiation. Mechanistically, HMGB2 can regulate the transcription of IL-6 and IL-1β through TUG1 and directly regulate the transcriptional level of TNF-α (Graphical abstract image by Figdraw).
Linoleic Acid Potentiates Response to Chemotherapy in Biliary Tract Cancer Through RARγ Activation
e71232 | First Published: 13 November 2025
Linoleic acid (LA) potentiates chemotherapy response in biliary tract cancer (BTC) by activating the nuclear receptor RARγ. In addition to inhibiting cell proliferation, the LA-RARγ axis drives a powerful dual response: promoting cancer cell apoptosis and enhancing antitumor immunity (Created with BioRender.com).
Open AccessLoss of the RNA Binding Protein HuR in Early Murine Limb Mesenchyme Does Not Affect Development but Leads to Impaired Bone Homeostasis in Adulthood
e71222 | First Published: 20 November 2025
The RNA-binding protein HuR (Elavl1) is essential for limb development. In germline HuR knockouts, apical ectodermal ridge signaling is lost, though mesenchymal signals persist. Mesenchyme-specific HuR deletion does not affect embryonic limbs, but adult mutants are affected and exhibit markedly reduced trabecular bone density. These findings point toward a critical role for HuR expression in nonmesenchymal tissues during limb development, but its presence in mesenchymal-derived cells is important for the healthy homeostasis of the mature limb skeleton. Created using BioRender.
Open AccessLipidome Plasticity Preserves Membrane Function in Sphingolipid‐Depleted HAP1 Cells
e71238 | First Published: 14 November 2025
Near-haploid HAP1-SPT cells, which cannot synthesize sphingolipids de novo, undergo a drastic reduction in sphingolipid content when grown under low FBS conditions. To compensate, they remodel their lipidome by increasing ether-linked phospholipids and adjusting glycerophospholipid saturation. Despite these changes, plasma membrane biophysical properties remain stable, highlighting lipidome plasticity as a key mechanism for preserving membrane homeostasis under sphingolipid depletion.
Oral Ingestion of Polystyrene Microplastics Aggravates Chronic Pancreatitis Through ROS Induced NF‐κb/TGF‐β Signaling Pathway and Alteration of Gut Microbiota
e71223 | First Published: 14 November 2025
Oral ingestion of microplastics (MPs) results in the deposition of MPs in the pancreas. Further, MPs can be absorbed by pancreatic stellate cells, stimulate the activation of cellular ROS, further activate NF-κB and TGF-β signaling pathways, and increase the levels of fibrosis-related proteins and collagen. Meanwhile, exposure to MPs alters gut microbial diversity, with downregulation of bacteria in the Bacteroidota phylum and upregulation of bacteria in the Verrucomicrobiota phylum.
Open AccessAn AMPK‐Centric Strategy: Foenumoside B Coordinates PINK1/Parkin‐Mediated Mitophagy With Nrf2/HO‐1 Antioxidant Signaling to Resolve Oxidative Stress in Radiation‐Induced Lung Injury
e71225 | First Published: 14 November 2025
In RILI, FSB directly activates AMPK, thereby driving PINK1/Parkin-mediated mitophagy and remodeling Nrf2-mediated redox homeostasis, which in turn reduces the generation and accumulation of ROS and suppresses DNA damage and senescence in epithelial cells.
Liraglutide Mitigates Renal Injury in Diabetic Kidney Disease by Suppressing Podocyte Cholesterol Accumulation Through mTOR/VMP1‐Regulated Autophagy
e71229 | First Published: 17 November 2025
Liraglutide inhibits mTOR to upregulate VMP1, thereby promoting autophagy and reducing podocyte cholesterol accumulation, ultimately ameliorating DKD.
FOXA1 Upregulates HILPDA to Enhance Lipid Droplet Accumulation and Anoikis Resistance in Lung Adenocarcinoma
e71249 | First Published: 17 November 2025
This study reveals that FOXA1, as a transcription factor, binds to the promoter of the HILPDA gene and significantly upregulates its expression. High HILPDA expression promotes lipid droplet accumulation, which not only provides additional energy and protection for cancer cells and enhances their resistance to anoikis, but also directly facilitates cell migration and invasion, thereby driving the metastasis of lung adenocarcinoma.
Open AccessSestrin2 Exerts a Novel Protective Effect Against LPS‐Induced Ferroptosis via the Nrf2–SLC7A11–GPX4 Signaling Axis
e71251 | First Published: 26 November 2025
This graphical abstract shows that LPS downregulates SESN2, leading to suppressed GPX4 activity, increased ROS, lipid peroxidation, and inflammation. SESN2 overexpression reverses these effects by activating the Nrf2/SLC7A11/GPX4 axis, reducing MDA and 4HNE levels, preserving redox balance, and alleviating ocular symptoms including hypopyon and retinal vascular inflammation.
Heat‐Induced Pathophysiological and Metabolic Changes at the Feto‐Maternal Interface Predisposing to Preterm Birth
e71252 | First Published: 17 November 2025
This study presents a comprehensive 2D in vitro heat exposure model using maternal decidual cells (DECs) and fetal amniotic epithelial cells (AECs) heat-treated cells at 39°C and subsequent downstream physiological and metabolic changes. Heat stress triggered physiological changes including mitochondrial dysfunction, indicated by reduced ATP production, and disrupted expression of key mitochondrial markers (HSPD1 and ATP5F1). Heat-induced oxidative stress was also evident (decreased intracellular GSH), which subsequently caused DNA damage, senescence, and inflammatory activation. Metabolic derangement was also evident following heat treatment.
Open AccessCentral Osmolality Sensing for Arginine Vasopressin Release Is Mediated by WNK1‐OSR1/SPAK‐Kv3.1 Cascade
e71213 | First Published: 17 November 2025
Extracellular hyperosmolality extracts water from the catalytic center of WNK1 increasing the kinase activity. WNK1 phosphorylates and activates OSR1/SPAK leading to increases in Kv3.1 activity. Enhanced Kv3.1 activity accelerates repolarization, increasing afterhyperpolarization (AHP) and/or shortening AP width to increase action potential firing.
D‐Dopachrome Tautomerase‐Driven Astrocytic CCL7 Aggravates Neuropathology by Recruitment of Microglia Following Spinal Cord Injury
e71248 | First Published: 17 November 2025
Graphical overview of the role and mechanism of D-DT-driven astrocytic CCL7 production following spinal cord injury in rats. SCI-induced D-DT binds to the CD74 receptor on astrocytes, promoting CCL7 production via activation of both the MAPK/NF-κB and IL-6/STAT3 signaling pathways. Astrocyte-derived CCL7 subsequently recruits microglia/macrophages to the lesion site by engaging the CCR2 receptor.
Open AccessDissecting Shared Genetic Architecture of Thoracic Aortic Aneurysm and Aortic Related Traits and Identifying SplA/Ryanodine Receptor Domain and SOCS Box Containing 1 Involved in Smooth Muscle Phenotype Switching and Cell Senescence Through Alternative Splicing
e71117 | First Published: 18 November 2025
The flowchart of the study. BAPN, β-aminopropionitrile; FUMA, Functional Mapping and Annotation; GO, Gene Ontology; GWAS, genome-wide association study; KEGG, Kyoto encyclopedia of genes and genomes; LDSC, LD score regression; MR-JTI, mendelian randomization joint-tissue imputation; MTAG, multi-trait analysis of GWAS; siRNA, small interfering RNA; SPSB1, SPRY Domain-Containing SOCS Box Protein 1; TAA, thoracic aortic aneurysm.
Metabolic Rigidity as a Mechanical Barrier to Malaria: Flickering Loss in PKLR‐Deficient Erythrocytes
e71234 | First Published: 19 November 2025
ATP-dependent membrane flickering in healthy red blood cells (RBCs) facilitates parasite invasion by maintaining cytoskeletal plasticity. In contrast, PKLR-deficient RBCs exhibit suppressed flickering due to impaired glycolysis, leading to increased membrane rigidity that acts as a mechanical barrier against Plasmodium entry. This biophysical phenotype reveals a potential nonimmunological defense mechanism in PKLR enzymopathy.
Elesclomol‐Induced Copper Influx Attenuates Lung Adenocarcinoma Progression With Involvement of the ER Stress/PCK2 Axis
e71250 | First Published: 18 November 2025
Schematic diagram of copper-induced cell death in LUAD. Elesclomol, as a copper ionophore, promotes copper influx into LUAD cells. This copper influx leads to cellular copper overload. Copper overload induces ER stress in LUAD cells. ER stress upregulates PCK2, which in turn inhibits the tricarboxylic acid (TCA) cycle. Collectively, these pathways orchestrate the cellular responses to excessive copper levels in LUAD cells, highlighting the complex interplay between copper homeostasis, metabolic reprogramming, and cell death mechanisms.
Swim Exercise Mitigates BCAA‐Induced Atrial Remodeling and AF Susceptibility via Inhibition of Bax‐Mediated Mitochondrial Apoptosis
e71227 | First Published: 20 November 2025
Atrial fibrillation (AF) is the most common sustained arrhythmia. Although elevated branched-chain amino acids (BCAA) are linked to cardiovascular disease, their specific role in AF was not well defined. This study shows that BCAA supplementation induces atrial remodeling and increases AF susceptibility in mice, with swim exercise reversing these effects. Mechanistically, besides causing insulin resistance, BCAA supplementation promoted AF by activating Bax-mediated apoptosis, thus identifying a critical mechanism behind this relationship.
Inhibition of H3K79me2 by DOT1L Inhibitor EPZ5676 Promotes Mouse Embryonic Lung Branching Morphogenesis via Increasing Epithelium Proliferation
e71257 | First Published: 18 November 2025
EPZ5676 inhibits DOT1L-mediated H3K79me2, promoting mouse embryonic lung branching morphogenesis. Treatment with EPZ5676 enhances the proliferation and differentiation of lung epithelial progenitor cells into mature epithelial lineages. EPZ5676 synergizes with FGF7 to drive pulmonary epithelium tissue enlargement and secondary branching. This epigenetic modulation promotes branching morphogenesis in mouse embryonic lungs, underscoring the therapeutic potential of EPZ5676 in lung development and related disorders.
Open Accessc‐Abl Kinase Targets Tight Junction Protein ZO‐2 in Regulation of Cell Migration and Morphology
e71214 | First Published: 19 November 2025
c-Abl binds and phosphorylates ZO-2 directly at its C-terminus and indirectly at the N-terminus via JAK1. These phosphorylation events weaken cytoskeletal contractility, lower traction forces, and reduce cell migration, establishing ZO-2 as a central mediator linking c-Abl activity to changes in cell morphology and motility.
LEF1 Suppresses Ferroptosis in Colorectal Cancer Cells by Targeted Promotion of SLC7A11 Transcription
e71231 | First Published: 19 November 2025
LEF1 suppresses ferroptosis in colorectal cancer cells by targeting SLC7A11 transcription.
Open AccessS1P3 Receptor Mediates the Proinflammatory Effect of the Endocannabinoid 2‐Arachidonoylglycerol in Endometriotic Epithelial Cells
e71255 | First Published: 26 November 2025
The endocannabinoid 2-arachidonoylglycerol (2-AG) induced a marked inflammatory response in human endometriotic epithelial cells. A functional cross talk between the signaling pathways of 2-AG and the bioactive sphingolipid sphingosine 1-phosphate (S1P) has been identified here in endometriosis. Indeed, the specific S1P receptor S1P3, whose expression is augmented by 2-AG, is crucial for transducing the biological action of the endocannabinoid. Notably, the functional cross talk was found to be independent of both isoforms of the S1P biosynthetic enzyme, sphingosine kinase (SK1/SK2).
MYST1‐Mediated Lysine Acetylation Stabilizes KLF4 to Promote Intimal Hyperplasia
e71247 | First Published: 21 November 2025
This study demonstrates that MYST1 knockdown attenuates neointima formation in rat carotid artery injury models and suppresses SMC proliferation and migration in cellular models. Mechanistically, MYST1 promotes neointima formation by stabilizing KLF4 via acetylation, which inhibits SRF-TAZ interaction, drives pathological SMC phenotypic switching, and ultimately accelerates vascular remodeling.
FFAR4 Functions as a DHA Receptor to Attenuate LPS‐Induced Inflammation via the cAMP/IκBα Pathway in Large Yellow Croaker (Larimichthys crocea)
e71068 | First Published: 20 November 2025
This schematic illustrates the proposed mechanism by which Ffar4 mediates the anti-inflammatory effects of DHA in response to lipopolysaccharide (LPS)–induced inflammation.
SAA1 Induces TGF‐β1 Secretion by Ovarian Cancer Cells, Leading to M2 Macrophage Polarization and Inhibition of NK Cell Activity
e71239 | First Published: 21 November 2025
This study found that high expression of SAA1 in ovarian cancer cells promotes the expression of TGF–β1, which in turn promotes macrophage M2 polarization and inhibits the killing ability of NK cells against tumor cells. In addition, this regulatory mechanism has also been validated in mice.
Open AccessDysregulated Fatty Acid Metabolism in Preeclampsia Among Highland Andeans: Insights Into Adaptive and Maladaptive Placental Metabolic Phenotypes
e71254 | First Published: 22 November 2025
Multi-omic profiling of highland Andeans reveals adaptive fetal haplotypes associated with favorable placental metabolic phenotypes, while preeclampsia is marked by dysregulated fatty acid oxidation and acylcarnitine accumulation across maternal-placental-fetal compartments. Metabolomic profiling showed widespread accumulation of medium- and long-chain acylcarnitines in preeclamptic cases versus normotensive controls, representing maladaptive and adaptive phenotypes, respectively. Adaptive fetal haplotypes, consisting of genes associated with lipid metabolism (CPT2/LRP8, EXOC4, LIPG) identified via integrative haplotype scores (iHS), were associated with healthier placental metabolic profiles. Created in BioRender (https://BioRender.com/j98qv87).
Open AccessCD8+ T Cells Negatively Modulate Ischemia‐Induced Angiogenesis in Mice
e71165 | First Published: 17 November 2025
Graphical illustration of the mechanism of CD8+ T-cells/IFN-γ axis-mediated angiogenesis in response to ischemic stress. CD8+ T-cell functions as an important mediator of ischemia-induced angiogenesis via the modulation of inflammation, oxidative stress, proteolysis, and endothelial proliferation that might be mediated by the IFN-γ/NLRp3-caspase-1 and VEGF/Erk1/2 axes. And EGCG administration can improve ischemia-induced angiogenesis by modulation of CD8+ T-cells/IFN-γ axis.
Ubiquitin Specific Peptidase 51 Exacerbates Skeletal Muscle Injury by Enhancing APAF1‐Mediated Apoptosis and Pyroptosis
e71242 | First Published: 22 November 2025
In the Skeletal Muscle Injury (SMI) microenvironment, Ubiquitin Specific Peptidase 51 (USP51) expression is significantly upregulated, functional studies uncovered that USP51 interacts with and deubiquitinates APAF1. APAF1 catalyzes caspase activation and prompts apoptosis and pyroptosis; hence, the USP51-APAF1 axis amplified SMI through apoptosis and pyroptosis.
BRG1 Ablation in Vascular Smooth Muscle Cells Ameliorates Abdominal Aortic Aneurysm: Mechanism and Translational Potential
e71199 | First Published: 22 November 2025
Vascular smooth muscle cell (VSMC)-derived BRG1 drives abdominal aortic aneurysm (AAA) progression. Mechanistically, BRG1 triggers VSMC phenotypic switching by activating CTSK transcription, leading to increased apoptosis and upregulation of MMP2/MMP9, key mediators of vascular remodeling in AAA.
Siramesine Attenuates Early Brain Injury Through the TMEM97/NPC1 Pathway After Experimental Subarachnoid Hemorrhage in Rats
e71237 | First Published: 23 November 2025
The graphical abstract depicts that Siramesine attenuates early brain injury after subarachnoid hemorrhage by modulating the TMEM97/NPC1/DJ-1 pathway, which suppresses Drp1-mediated mitochondrial fission and neuronal apoptosis.
CD8+ T Cell Cytotoxicity and Exhaustion Underlie Liver Allograft Rejection: Insights From a Murine Transcriptomic Atlas
e71259 | First Published: 24 November 2025
Unveiling the molecular mechanisms of liver transplantation (LT) rejection versus tolerance remains crucial. Using murine orthotopic LT models, we performed graft transcriptomic profiling. Rejection was characterized by 2560 differentially expressed genes, highlighting T cell receptor signaling and cytokine interaction. Hub genes (e.g., Cd8a, Gzmb, Pdcd1, Lag3) revealed CD8+ T cell cytotoxicity and exhaustion were pivotal, confirmed by elevated PD-1/TIM-3 and granzyme B. This dynamic balance provides new insights into rejection mechanisms and potential therapeutic targets.
Neuronal GSK3β Protects Against Amyloid Pathology by Regulating APP Degradation
e71267 | First Published: 23 November 2025
Schematic illustrating the regulation of APP degradation by neuronal GSK3β in 5 × FAD mice. In the 5 × FAD model, GSK3β promotes APP degradation. Conditional knockout of Gsk3β impairs this process, resulting in APP accumulation. This leads to increased Aβ plaque formation and enhanced neuroinflammatory responses.
Microglial Nrf2 Functions as a Cell‐Autonomous Regulator of Neuroinflammation and Trained Immunity in the Aging Brain
e71244 | First Published: 25 November 2025
Age-related decline in microglial Nrf2 promotes inflammatory activation, antigen presentation, CD4+ T cell infiltration, and trained immunity, driving disease-associated microglia phenotypes and resulting in cognitive deficits and increased susceptibility to neurodegeneration.
Unraveling the Role of PTGIR in Atrial Fibrillation: Insights From Single‐Cell Sequencing and Mendelian Randomization
e71200 | First Published: 25 November 2025
Single-cell RNA sequencing of 47 565 atrial cells revealed fibroblast-centered signaling in atrial fibrillation. Mendelian randomization identified COL6A2 and PTGIR as protective genes, while SERPINE1 and VIM were risk genes. Validation in a rat model confirmed PTGIR expression and fibrosis markers, suggesting PTGIR as a protective factor against atrial fibrosis.
Role of TRPV6‐Mediated Calcium Signaling in High‐Glucose–Inhibited Keratinocyte Migration
e71270 | First Published: 25 November 2025
High glucose reduced TRPV6 expression, Ca2+ influx and cell migration in keratinocytes. Mechanistically, a high-glucose environment reduced TRPV6 expression and TRPV6-mediated Ca2+ influx, which eventually inhibited the migration of keratinocytes through a CaM-AKT-FN1 pathway.
RESEARCH LETTER
Cardiac Chamber‐Specific Regulation of Myosin Biochemical Super‐Relaxation and Auto‐Inhibition
e71265 | First Published: 22 November 2025
The combination of Mant-ATP (2′-(or-3′)-O-(N-Methylanthraniloyl) Adenosine 5′-Triphosphate) chase experiments and all-atomistic molecular dynamics simulations, revealed that myosin auto-inhibition and energetic super-relaxation differ between chambers (within atrial or ventricular cardiomyocytes).
Open AccessIL‐1β Upregulates PD‐L1 in Small Extracellular Vesicle of Endothelial Origin
e71272 | First Published: 23 November 2025
PD-L1 is crucial to the regulation of immune cells and rises in response to inflammation in HUVECs. We studied PD-L1 expression on sEVs in HUVECs and explored its modulation in response to IL-1β, a key player in the immune response and involved in the pathogenesis of several diseases. sEVs were collected by sequential ultracentrifugation from HUVEC (±IL-β) and characterized by NTA, electron microscopy and WB. The workflow highlights that IL-1β leads to the release of a greater quantity of sEVs-PD-L1+.
CORRECTION
Free AccessCorrection to “OTUB1 Modulates Ferroptosis by Regulating SLC7A11 Ubiquitination in Pancreatic β‐Cells”
e71233 | First Published: 25 November 2025
This article is a correction.
Free AccessCorrection to “Transcriptomic and DNA Methylomic Defects in In Vitro Matured Lamb Oocytes and Potential Improvement of Their Development by Supplementing Phorbol Myristate Acetate During In Vitro Maturation”
e71276 | First Published: 21 November 2025
This article is a correction.