生物学最新文献

{"title":"Correction.","authors":"","doi":"10.1080/13510002.2026.2648349","DOIUrl":"10.1080/13510002.2026.2648349","url":null,"abstract":"","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2648349"},"PeriodicalIF":7.4,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13015051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147504926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating ancestry adjustment in multi-ancestry epigenome-wide analysis.","authors":"Yueming Liu, Alan Kuang, Marie-France Hivert, William L Lowe, Jami L Josefson, Denise M Scholtens","doi":"10.1080/15592294.2026.2646063","DOIUrl":"10.1080/15592294.2026.2646063","url":null,"abstract":"<p><p>Proper adjustment for population substructure is essential in epigenome-wide association studies (EWAS), particularly in cohorts with diverse ancestries. EPISTRUCTURE offers a genotype-free approach to ancestry inference, originally developed using a European reference population from the Cooperative Health Research in the Region of Augsburg (KORA) study. However, its effectiveness in genetically diverse, multi-ancestry cohorts remains insufficiently evaluated. For EWAS using cord-blood samples from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study, we systematically assessed the ancestry adjustment performance of EPISTRUCTURE principal components (PCs) derived from the widely used KORA-based reference set versus new reference sets generated from genotyping data of the multi-ancestry HAPO cohort. HAPO-based reference sets were defined by varying SNP - CpG <math><mrow><msup><mi>R</mi><mn>2</mn></msup></mrow></math> thresholds (e.g. RS30: <math><mrow><msup><mi>R</mi><mn>2</mn></msup></mrow><mo>></mo><mn>0.3</mn></math>) to identify ancestry-informative CpGs. We applied these reference sets for population substructure adjustment in EWAS of three newborn adiposity traits, birthweight, cord C-peptide, and sum of skinfolds, to evaluate their impact on association detection and biological interpretation. Compared to the KORA reference, the HAPO RS30 reference consistently produced lower genomic inflation and identified more biologically relevant associations for birthweight and cord blood C-peptide in EWAS of HAPO cord blood samples (<i>n</i> = 3,116). Pathway enrichment analyses revealed strong immune and metabolic signals, including pathways uniquely captured by EWAS when using the HAPO-derived reference for ancestry adjustment. Trait enrichment using the EWAS Catalog further confirmed associations with fetal growth, maternal metabolic traits, and glucose regulation. Our findings demonstrate that reference sets derived from multi-ancestry cohorts like HAPO better capture underlying population substructure and improve ancestry adjustment in diverse EWAS settings.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2646063"},"PeriodicalIF":3.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147485090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"M6A-dependent regulation of microRNAs from CKD stage 5 patients: insights from epigenetic modification analysis.","authors":"Zhiqian Yang, Fanna Liu, Mingjun Ye, Qiang Yan, Zhipeng Zeng, Jingsheng Ma, Haitao Li, Hualin Ma, Xinzhou Zhang, Xiaofeng Zhu, Yong Dai, Donge Tang","doi":"10.1080/15592294.2026.2653962","DOIUrl":"10.1080/15592294.2026.2653962","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) stage 5 is frequently accompanied by systemic inflammation, and peripheral blood mononuclear cells (PBMCs) play an important role. To define the epitranscriptomic features of PBMC small RNAs in CKD stage 5, we profiled N6-methyladenosine (m6A) using small RNA modification microarrays. A total of 158 miRNAs, 149 pre-miRNAs, and 197 tsRNAs showed differential m6A modification. Enrichment analysis implicated PI3K-Akt, p53 signalling, and leukocyte transendothelial migration. Integrating target prediction with GEO transcriptomic datasets identified IRF1 and RUNX2 as key targets. MeRIP confirmed reduced m6A in miR-205-3p and miR-93-5p, accompanied by upregulation of RUNX2 and downregulation of IRF1 by qPCR. These results define an altered m6A-modification profile of PBMC small RNAs in CKD stage 5 and highlight miRNA-target gene axes with potential biomarker utility.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2653962"},"PeriodicalIF":3.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147632646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bilirubin reduces mortality in sepsis models by inhibiting NOX2-mediated formation of neutrophil extracellular traps.","authors":"Sang-Jin Kim, Chang Woo Ko, Wan-Seo Kim, Yeon Jun Kang, Chul-Hwan Lee, Won-Woo Lee, Jong-Wan Park","doi":"10.1080/13510002.2026.2664962","DOIUrl":"10.1080/13510002.2026.2664962","url":null,"abstract":"<p><strong>Objectives: </strong>Sepsis is a life-threatening condition driven by a dysregulated immune response to infection, yet therapeutic options beyond antibiotics and vasopressors remain limited. Neutrophil extracellular traps (NETs) contribute significantly to sepsis-induced tissue injury, and NETosis inhibition has emerged as a potential therapeutic strategy. We hypothesized that the endogenous metabolite bilirubin mitigates inflammation in sepsis by inhibiting NETosis through targeting NOX2.</p><p><strong>Methods: </strong>Two murine sepsis models were used to assess the effects of bilirubin on survival and systemic NETosis. Plasma NET biomarkers were quantified, and primary human neutrophils were used to validate the NETosis-inhibitory activity of bilirubin <i>in vitro</i>. Mechanistic studies included ROS measurements, NOX2 loop C mutational analysis, and inhibition of endocytosis and autophagy to examine how bilirubin modulates NOX2 stability.</p><p><strong>Results: </strong>Bilirubin improved survival and reduced NET biomarkers in both models. It inhibited NETosis in human neutrophils by suppressing ROS-dependent NETosis and promoting the internalization and degradation of NOX2 via endocytosis and autophagy.</p><p><strong>Discussion: </strong>These findings identify bilirubin as an endogenous inhibitor of NETosis. By targeting NOX2 and suppressing NETosis, bilirubin may represent a promising therapeutic candidate for sepsis management.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2664962"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147779252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neutralizing epitope mapping for deltacoronavirus receptor-binding domain and seroepidemiological survey across different animal species.","authors":"Dexin Li, Liying Hao, Baicheng Huang, Zhiyan Wang, Zenglin Wang, Menghao Guo, Yunjing Zhang, Junhua Deng, Yufang Li, Shaoruo Zhao, Kegong Tian, Xiangdong Li","doi":"10.1080/21505594.2026.2668161","DOIUrl":"10.1080/21505594.2026.2668161","url":null,"abstract":"<p><p>Porcine deltacoronavirus (PDCoV) is an emerging enteric pathogen that poses a significant threat to the global swine industry and carries a potential public health risk. The development of neutralizing monoclonal antibodies (mAbs) is crucial for preventing and controlling PDCoV. However, research on neutralizing linear epitopes within the PDCoV receptor-binding domain (RBD) and the establishment of serological assays based on such mAbs remains limited. In this study, we generated two neutralizing mAbs, 1C12 and 3A11, targeting the PDCoV RBD. Epitope mapping revealed that 1C12 recognizes a linear epitope (³¹⁶DFGEARLD³²³), whereas 3A11 binds to a conformational epitope. Further residue analysis identified Arg321 as the most critical residue for binding to 1C12. Additionally, the integrity of the entire ³²¹RLD³²³ motif was found to be indispensable for the conformational recognition by mAb 3A11. Using these mAbs, we developed two blocking enzyme-linked immunosorbent assay (bELISA) methods (bELISA-1C12 and bELISA-3A11). Evaluation of 150 clinical samples demonstrated that bELISA-1C12 exhibited 93.3% concordance with a virus neutralization test (VNT), indicating higher diagnostic sensitivity than bELISA-3A11 (92.7%). A large-scale serosurvey of pig populations across ten Chinese provinces in 2025, conducted using bELISA-1C12, revealed a PDCoV seropositivity rate of 13.6%. Notably, when extending the serological screening to 21 additional animal species, we detected PDCoV antibodies in peafowl serum for the first time, suggesting possible exposure to the virus. This study identifies key antigenic epitopes on the PDCoV RBD and provides valuable tools for epidemiological surveillance and assessing the transmission risk of PDCoV.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"17 1","pages":"2668161"},"PeriodicalIF":6.8,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13166184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147843543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sirtuin 5-mediated desuccinylation of PRDX6 inhibits ferroptosis and alleviates sepsis-associated acute kidney injury.","authors":"Wenlong Lin, Caitao Dong, Qinhong Jiang, Yuanquan Lou, Long Wang, Ziqi He","doi":"10.1080/13510002.2026.2657075","DOIUrl":"10.1080/13510002.2026.2657075","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the role of the SIRT5-PRDX6 axis during the pathogenesis of sepsis-associated acute kidney injury (SA-AKI).</p><p><strong>Methods: </strong><i>In vivo</i> and <i>in vitro</i> sepsis models were established to evaluate oxidative stress and inflammatory responses. High-throughput proteomics analysis identified ferroptosis as a key mechanism underlying SA-AKI. The levels of HMOX1, NQO-1, GPX4, ACSL4, Fe²⁺, IL-1β, TNF-<i>α</i>, MDA, and GSH were measured. SIRT5 knockdown/overexpression experiments were performed in HK-2 cells, and SIRT5-deficient mice were used to explore its regulatory role. Co-immunoprecipitation (Co-IP) and site-directed mutagenesis verified SIRT5-PRDX6 interaction and desuccinylation sites.</p><p><strong>Results: </strong>Ferroptosis was critical in SA-AKI progression. In LPS-induced HK-2 cells, HMOX1, NQO-1, ACSL4, Fe²⁺, IL-1β, TNF-<i>α</i>, and MDA were significantly increased, whereas GSH and GPX4 were downregulated. Treatment with ferrostatin-1 (Fer-1) attenuated ferroptosis and oxidative damage. SIRT5 decreased in a time-dependent manner following LPS stimulation. SIRT5 knockdown exacerbated LPS-induced ferroptosis, whereas SIRT5 overexpression suppressed it. SIRT5 activation alleviated AKI in mice, whereas SIRT5 deficiency aggravated it. Mechanistically, SIRT5 desuccinylated PRDX6 at lysine 209, thereby inhibiting inflammatory and oxidative stress responses, attenuating ferroptosis, and ultimately ameliorating renal injury.</p><p><strong>Conclusion: </strong>The SIRT5-PRDX6 axis regulates SA-AKI pathogenesis by modulating ferroptosis and represents a novel potential therapeutic target.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2657075"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13072693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Type III intermediate filaments as novel CoAlation targets.","authors":"Nuria Goya-Iglesias, Bess Yi Kun Yu, Ivan Gout, Dolores Pérez-Sala","doi":"10.1080/13510002.2026.2692797","DOIUrl":"10.1080/13510002.2026.2692797","url":null,"abstract":"<p><strong>Objectives: </strong>Type III intermediate filaments, such as vimentin, GFAP, and desmin, are involved in cell mechanics, signaling, and stress responses, and are tightly regulated by posttranslational modifications (PTMs). The monomers of these proteins possess a single cysteine residue that plays a key role in network remodeling under oxidative stress. CoAlation is a PTM involving mixed disulfide bond formation between a protein thiol and the coenzyme A (CoA) thiol. Here we aim to investigate the potential CoAlation of vimentin, GFAP, and desmin, and its functional consequences.</p><p><strong>Methods: </strong>CoAlation of type III intermediate filaments and its interplay with other oxidative modifications was assessed in vitro by gel assays and immunological detection, whereas its effect on vimentin filament assembly was evaluated by electron microscopy. In cells, CoAlation was evaluated by CoA immunofluorescence, proximity ligation assay, and/or immunoprecipitation.</p><p><strong>Results: </strong>CoAlation of vimentin, GFAP, and desmin occurs in vitro and in cells, and is enhanced by oxidants. In the case of vimentin, CoA reciprocally influences other thiol group modifications in vitro, attenuating disulfide-mediated oligomerization and cysteine alkylation. Moreover, in vitro polymerization in the presence of CoA results in shorter vimentin filaments.</p><p><strong>Conclusion: </strong>We show that vimentin, GFAP, and desmin are CoAlated at their single cysteine residues. Our results suggest that CoAlation may influence filament assembly and compete with other cysteine modifications. Moreover, given its reversibility, CoAlation could potentially play a protective role against more deleterious modifications, such as irreversible cysteine oxidation.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2692797"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13307387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cr(VI) and DON co-exposure triggers intestinal epithelial cells ferroptosis and pyroptosis through Nrf2/NF-κB/NLRP3 to impair intestinal barrier function.","authors":"Yueming Gu, Xinyuan Miao, Linrui Fan, Guodong Cai, Ruilong Song, Hui Zou, Jianhong Gu, Yan Yuan, Xuezhong Liu, Zongping Liu, Jianchun Bian","doi":"10.1080/13510002.2026.2724639","DOIUrl":"10.1080/13510002.2026.2724639","url":null,"abstract":"<p><strong>Objectives: </strong>Cr(VI) and DON are natural co-occurring pollutants in the environment. This study aimed to investigate the molecular mechanisms underlying oxidative damage to the intestinal barrier and intestinal epithelial cell (IECs) toxicity induced by Cr(VI) and DON.</p><p><strong>Methods: </strong>The target genes and signaling pathways were predicted using the network toxicology method. This was verified through cell intervention experiments with Nrf2 activator TBHQ, NF-κB inhibitor PDTC, and NLRP3 inhibitor MCC950.</p><p><strong>Results: </strong>Cr(VI) and/or DON aggravated inflammatory infiltration in the intestine, disrupted tight junction structures. Network toxicology revealed that ferroptosis and pyroptosis pathways are involved in regulating oxidative damage and barrier dysfunction in primary small IECs in broilers. Cr(VI) and/or DON induced oxidative stress and inhibited Nrf2 expression. They abnormally activated the NF-κB/NLRP3 pathway in IECs, thereby triggering ferroptosis and pyroptosis, and exacerbating oxidative damage to the intestinal barrier. Overexpression of Nrf2 and silencing of NLRP3/NF-κB could bidirectionally reverse oxidative stress, iron accumulation, inflammatory factor secretion and intestinal barrier dysfunction in IECs, inhibit the progression of ferroptosis and pyroptosis.</p><p><strong>Conclusion: </strong>The cross-regulation of ferroptosis and pyroptosis mediated by the bidirectional imbalance of the Nrf2/NF‑κB/NLRP3 axis constitutes the core molecular mechanism underlying intestinal epithelial barrier dysfunction and oxidative damage induced by co-exposure to Cr(VI) and DON.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2724639"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13543835/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148888481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The mRNA architecture of the translation termination site primes programmed stop codon readthrough events in <i>Drosophila</i>.","authors":"Laveena Kansara, Georg Wolfstetter, Daniel Wintermayr, Ioannis Alexopoulos, Alejandra Escos, Marc Friedländer, Ylva Engström","doi":"10.1080/15476286.2026.2667707","DOIUrl":"10.1080/15476286.2026.2667707","url":null,"abstract":"<p><p>Programmed stop codon readthrough (SCR) is a form of genetic re-coding, in which a near-cognate tRNA base-pairs with a stop codon, leading to the translation of a C-terminally extended protein. Recent studies revealed that SCR represents an evolutionarily conserved, spatio-temporally controlled mechanism of posttranscriptional gene regulation that requires <i>cis</i>-regulatory elements as well as <i>trans</i>-acting factors. In this study, we characterized <i>cis</i>-regulatory elements controlling programmed SCR of the <i>Drosophila</i> POU3-family member <i>drifter/ventral veins lacking</i> (<i>dfr/vvl</i>). Using S2 cell-based luciferase assays, we show that stop codon identity and the +4 to +9 nucleotide sequence are required but not sufficient for <i>dfr</i> SCR regulation. Phylogenetic prediction identified an mRNA stem-loop in the 3' UTR, proximal to the readthrough UAG codon. Mutational analysis revealed that the distance from the stop codon as well as stem-loop stability, but not the underlying sequence identity, critically impact <i>dfr</i> SCR. Similarly, the mRNA stem-loop promoted SCR in an <i>in vivo Drosophila</i> model. We applied this information to refine computational prediction of SCR-associated mRNA stem-loops and show that these elements effectively promote SCR of heterologous mRNAs. These findings increase our understanding of SCR and the underlying regulatory mechanisms.</p>","PeriodicalId":21351,"journal":{"name":"RNA Biology","volume":" ","pages":"1-21"},"PeriodicalIF":4.1,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13170385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147842295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EGCG-loaded nanoparticles attenuate post-SAH white matter injury by targeting HO-1/S100A10 to suppress oxidative stress-induced reactive astrocytes.","authors":"Dongcen Lang, Yanning Zheng, Jing Zhang, Zheng Li, Mengyu Niu, Jian Wang, Xue Wang, Liyong Huang, Jiangyu Xue, Li Li, Ying Chen","doi":"10.1080/13510002.2026.2664955","DOIUrl":"10.1080/13510002.2026.2664955","url":null,"abstract":"<p><strong>Objective: </strong>Subarachnoid hemorrhage (SAH) is associated with high mortality and poor outcomes, which are closely related to white matter injury (WMI). (-)-Epigallocatechin-3-gallate (EGCG) exerts neuroprotective effects by inhibiting oxidative stress-related ferroptosis in astrocytes and improving neurological function. However, the role and mechanism of EGCG in regulating reactive astrocytes (RAs) to alleviate WMI after SAH remain unclear.</p><p><strong>Methods: </strong>A mouse model of SAH was used to evaluate the effects of EGCG-loaded nanoparticles (EGCG-NPs). Western blot, qPCR, and immunofluorescence were performed for biochemical analysis. Neurological function was assessed using neurological deficit scores and the Morris water maze test.</p><p><strong>Results: </strong>Following SAH, HO-1-mediated iron accumulation and ROS production promoted A1/A2 reactive astrocyte polarization, resulting in myelination damage and aggravated WMI. Knockdown of S100A10 inhibited iron-dependent oxidative stress in RAs and attenuated WMI. EGCG-NPs significantly suppressed HO-1/S100A10-mediated iron overload and oxidative stress in both A1 and A2 RAs, thereby alleviating WMI after SAH.</p><p><strong>Conclusion: </strong>EGCG-NPs attenuate SAH-induced WMI by inhibiting the iron overload-activated HO-1/S100A10 axis in RAs, representing a promising therapeutic strategy.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2664955"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147779390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}