Free Radical Biology and Medicine最新文献

{"title":"Aldehyde Dehydrogenase ALDH3A1 Rescues Cigarette Smoke-induced Emphysema by Conferring Alveolar Type 2 to Type 1 Cell Transition.","authors":"Jiajing Cui, Shuai Han, Jiachen Li, Xiaobo Li, Lirong Liang","doi":"10.1016/j.freeradbiomed.2025.10.002","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2025.10.002","url":null,"abstract":"<p><p>Cigarette smoke (CS) is one of the major risk factors of emphysema, which is characterized by alveolar destruction. Alveolar type 2 (AT2) cells enable regeneration of alveoli after injury by transiting into alveolar type 1 (AT1) cells; however, the mechanisms regulating AT2 to AT1 transition during the CS-induced emphysema remain unclear. Primary human alveolar cells exposed to commercially available cigarette smoke extract (CSE) were subjected to single-cell RNA sequencing, and data showed an imbalance in the ratio of AT1 to AT2 cells, with decreased expression of aldehyde dehydrogenase 3 family member A1 (ALDH3A1) in alveolar epithelial cells. Subsequently, a CS-induced emphysema mouse model was established using a nasal-oral exposure system. Compared to the control, the pulmonary function of CS-exposed mice was significantly reduced, and the alveolar structure was severely damaged with a significantly increased mean linear intercept. The ratio of aquaporin 5⁺ AT1 cells to surfactant protein C⁺ AT2 cells was significantly decreased, accompanied by the decreased expression of ALDH3A1. Additionally, in vitro models of CSE-induced emphysema and ALDH3A1 overexpression were established using alveolar organoids. Gene expression levels of ALDH3A1 in the organoids decreased with CSE exposure in a dose-dependent manner, and this decrease was transcriptionally regulated by aryl hydrocarbon receptor (AHR)/AHR nuclear transporter (ARNT). More critically, overexpression of ALDH3A1 or the AHR agonist, indole-3-pyruvic acid, effectively restored the ratio of NAD⁺/NADH and protected alveolar organoids against CSE-induced imbalance between AT1 and AT2 cells. This study confirms the crucial role of AHR/ARNT/ALDH3A1 signaling in maintaining alveolar structure during alveoli repair in CS-induced emphysema. The murine alveolar organoid successfully resembles the alteration in human lungs, providing a useful in vitro model to study the mechanism of emphysema.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the PRSS3-PAR2-ERK1/2 Axis Inhibits Malignancy and Regulates Chemosensitivity and Resistance through Ferroptosis in Breast Cancer.","authors":"Rongmeng Tian, Duoduo Li, Chunyan Lan, Hanli Xu, Xiaonan Ma, Daichuan Chen, Enkai Wang, Jun Liu, Tian Tian, Huafang Gao, Jiaqiang Huang","doi":"10.1016/j.freeradbiomed.2025.10.003","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2025.10.003","url":null,"abstract":"<p><p>Breast cancer (BRCA) heterogeneity contributes to malignancy progression and therapeutic resistance, yet the role of proteases in this process remains elucidated. In this study, we identified serine protease 3 (PRSS3), an indispensable member of the serine protease family, as an oncogenic driver in BRCA through its ability to inhibit ferroptosis. Immunohistochemical analysis of 90 paired BRCA tissue samples revealed high PRSS3 expression in 76.47% of HER2-positive subtypes, 87.30% of luminal A/B cases, and 90% of TNBC tumors. Elevated PRSS3 levels were significantly associated with advanced clinical stages, lymph node metastasis, and increased Ki-67 expression. Transcriptomic analysis integrated with functional studies using gain- and loss-of-function BRCA cell models demonstrated that PRSS3 promotes tumor progression mainly attributed to its splicing isoform 1 (PRSS3-V1), which interacted with protease-activated receptor 2 (PAR2) and enhances ERK1/2 phosphorylation both in vitro and in vivo. Silencing PRSS3 significantly induced cell cycle arrest and ferroptotic cell death via multiple mechanisms, including increased levels of malondialdehyde and lactate dehydrogenase levels, accumulation of labile iron via regulation of transferrin receptor 1 (TfR1) and ferritin heavy chain 1 and reactive oxygen species, mitochondrial membrane dysfunction, and activation of NLRP3 inflammasome. These effects were mediated by downregulation of SLC7A11 and GPX4, two key regulators of ferroptosis, resulting in increased lipid peroxidation. Treatment with the PAR2 agonist SLIGKV-NH2 or the TfR1 inhibitor ferrostatin II attenuated these effects. Furthermore, PRSS3 knockdown improved chemosensitivity to paclitaxel and doxorubicin and alleviated resistance to trastuzumab in BRCA cells. Our findings uncover a novel PRSS3-mediated mechanism underlying ferroptotic evasion in BRCA. Targeting the PRSS3-PAR2-ERK1/2 axis may offer therapeutic potential, with PRSS3-V1 serving as a valuable biomarker for BRCA subtype stratification.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone H3 acetylation reverses radioresistance in breast cancers through BRD3-mediated inhibition of RAD51 and inducing ferroptosis.","authors":"Dong-Man Ye, Yusong Qiu, Jiu-Mei Cai, Tao Yu, Yong Zhang","doi":"10.1016/j.freeradbiomed.2025.10.005","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2025.10.005","url":null,"abstract":"<p><p>Radiotherapy is a crucial treatment for patients undergoing breast cancer surgery, especially for those with locally advanced stage of breast cancers. However, low radiosensitivity significantly limits the efficacy of radiotherapy. Epigenetic regulation plays a critical role in cancer treatment, and histone H3 lysine acetylation (H3ac) affects the redox balance during homeostasis. Bromodomain-containing protein 3 (BRD3) is an H3ac reader, and its overexpression is associated with invasion, metastasis, and chemoresistance. However, its correlation with radiosensitivity remains unclear. Here, we reported that radiotherapy induced a significant increase in BRD3 level, whereas deacetylase inhibitors reduced BRD3 expression. ChIP-seq results showed that BRD3 binds to the RAD51 promoter region, which is involved in radioresistance, inhibiting RAD51 transcription and translation. Furthermore, the inhibition of RAD51 was mainly observed in the cytoplasm, revealing a novel mechanism in which RAD51 forms a complex with GPX4 and FTH1 to synergistically regulate ROS production. These findings suggest that H3ac regulates BRD3 expression, promoting ROS accumulation through the RAD51-mediated ferroptosis signaling pathway, reversing radioresistance and enhancing radiosensitivity.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative Stress and Multiple Sclerosis: trajectories and possible predictive activities of Pro and Antioxidant biomolecules.","authors":"V Bellisario, G Squillacioti, P Valentino, L Marozio, A Bertolotto, R Bono","doi":"10.1016/j.freeradbiomed.2025.09.052","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2025.09.052","url":null,"abstract":"","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiRNA-27a-5p alleviates diabetic vascular injury via modulating autophagy by targeting NOX4.","authors":"Yiwen Wang, Jian Zhang, Yang Gao, Shiyu Hu, Jingpu Wang, Ya'nan Qu, Ji'e Yang, Rong Huang, Hongbo Yang, Wenyuan Zheng, Chenguang Li, Feng Zhang, Jiatian Cao, Junbo Ge","doi":"10.1016/j.freeradbiomed.2025.09.057","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2025.09.057","url":null,"abstract":"<p><p>Diabetes mellitus (DM) presents significant public health challenges due to its contribution to high rates of disability and mortality through vascular complications. While many microRNAs (miRNAs) regulate endothelial homeostasis and contribute to vascular repair, their roles in diabetic endothelial injury have not been fully elucidated. Among these, miRNA-27a-5p (miR-27a-5p) is abundant in endothelial cells; yet its specific function in the context of diabetes remains unclear. This study specifically investigates the protective role of miR-27a-5p against diabetic vascular injury and its effects on autophagy and endothelial cell function. We observed that hyperglycemia-induced advanced glycation end-products (AGEs) induce excessive apoptosis and autophagy, leading to endothelial dysfunction by mediating reactive oxygen species (ROS) production. MiR-27a-5p overexpression promotes blood flow recovery in diabetic mice following hindlimb ischemia (HLI) through alleviating excessive autophagy and restoring endothelial dysfunction. Utilizing RNA sequencing and miRwalk analyses, we identified NADPH oxidase 4 (NOX4) as a direct target of miR-27a-5p. AGEs induce NOX4 expression, whereas miR-27a-5p post-transcriptional repress the elevation. Mechanistically, NOX4 regulates autophagy through the activation of MAPK signaling. Silencing NOX4 improved AGE-induced endothelial function by regulating apoptosis and autophagy. Collectively, these findings underscore the protective role of miR-27a-5p against vascular injury by modulating NOX4, highlighting it as a promising therapeutic target for the management of diabetic vascular complications.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MOTS-c attenuates mitochondrial dysfunction induces pyroptosis and cartilage degradation in osteoarthritis via an Nrf2-Dependent Mechanism.","authors":"Kechi Li, Tao Yang, Feiyu Chen, Chao Lou, Yanlin Chen, Zhenzhong Chen, Lin Ye, Xiaolong Sun, Guoxiang Liu, Chenglong Xie, Jiawei Fang, Xingyu Hu, Ye Zhu, Bin Liu, Dengwei He, Haiwei Ma","doi":"10.1016/j.freeradbiomed.2025.09.056","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2025.09.056","url":null,"abstract":"<p><p>Osteoarthritis, a common chronic degenerative disease in the field of orthopedics, is caused by the interaction of mechanical stress, traumatic inflammation, and metabolic imbalance, and this interaction progresses over time. MOTS-c, a mitochondria-derived peptide, exerts pivotal roles in regulating metabolism, anti-inflammation, and antioxidant stress responses. However, current research on the role of MOTS-c in osteoarthritis remains scarce, and its specific mechanism of action remains unclear. Therefore, this study aims to further explore the molecular mechanisms by which MOTS-c regulates osteoarthritis. Exogenous supplementation of MOTS-c improves mitochondrial dysfunction, inhibits the activation of inflammatory bodies and rescues chondrocyte pyroptosis, thereby regulating the metabolic balance of extracellular matrix (ECM). Mechanistically, MOTS-c plays a key role in LPS-induced oxidative stress and chondrocyte pyroptosis through the Nrf2/TXNIP/NLRP3 axis. Our research demonstrates that MOTS-c can not only effectively inhibit the expression of inflammatory factors but also promote the expression of major components of the extracellular matrix (ECM) and suppress the production of matrix metalloproteinases. We validated the in vivo efficacy of MOTS-c by establishing a murine osteoarthritis model. Analysis of imaging and histopathological results revealed that MOTS-c can effectively delay the degeneration of articular cartilage and ameliorate the progression of osteoarthritis. Collectively, our findings uncover the intrinsic regulatory mechanism of MOTS-c in chondrocytes and its potential value in the treatment of osteoarthritis.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms and Targeted Intervention of Mitochondria-Dependent Ferroptosis and Abnormal Ductular Reaction Caused by Benzo(a)pyrene.","authors":"Xinru Du, Sisi Song, Jing Wang, Hongquan Zhang, Yue Ma, Zhendong Wang, Qinliang Mo, Mengyue Ji, Sha Liu, Ziyi Wang, Moyan Wang, Chunxiao Zhou, Yuan Li, Chengwu Tang","doi":"10.1016/j.freeradbiomed.2025.10.001","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2025.10.001","url":null,"abstract":"<p><p>Chronic hepatobiliary diseases (CHDs), the second leading disease burden worldwide, are closely related to the occurrence and development of abnormal ductular reaction (DR). Tobacco smoking is an important pathogenic risk factor for CHDs, however, the functions and molecular mechanisms underlying in the tobacco smoking-induced abnormal DR, remain largely uninvestigated. Benzo[a]pyrene (B[a]P) is a representative hepatobiliary toxic substance among tobacco carcinogens. Our present study revealed that, B[a]P drove the DR occurrence through inducing the ferroptosis in bile duct epithelial cells (BECs). For the molecular mechanisms, the metabolic activation product of B[a]P, benzo[a]pyrene diol epoxide (BPDE) could directly bind to the Lys123 site of 14-3-3ε protein, which in turn inhibited its ubiquitination degradation. The abnormally elevated 14-3-3ε in turn activated voltage dependent anion channel 1 (VDAC1) through phosphoserine binding/regulation, leading to an abnormal coupling between endoplasmic reticulum (ER) and mitochondria. The shortened distance between the ER and mitochondria caused the mitochondrial Ca²⁺ overload, inducing the overproduction of reactive oxygen species (ROS). These processes ultimately caused the ferroptosis in BECs and initiated the DR progression. In terms of targeted intervention, we further innovatively screened and identified a small molecule of traditional Chinese medicine monomer, quercetin, which could efficiently target the phosphoserine binding region of 14-3-3ε protein. Finally, we confirmed that targeted intervention of 14-3-3ε by quercetin significantly inhibited the B[a]P-induced ferroptosis and abnormal DR.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PIM-1 exacerbates sepsis-associated encephalopathy via promoting microglia NLRP3 inflammasome activation","authors":"Xiaomeng Ji ,&nbsp;Jingquan Dong ,&nbsp;Wenting Zhu ,&nbsp;Shasha Zhang ,&nbsp;Yaru Chen ,&nbsp;Xiao Liu ,&nbsp;Yan Cao ,&nbsp;Panpan Zhao ,&nbsp;Zibo Dong","doi":"10.1016/j.freeradbiomed.2025.09.055","DOIUrl":"10.1016/j.freeradbiomed.2025.09.055","url":null,"abstract":"<div><h3>Background</h3><div>Sepsis-associated encephalopathy (SAE) represents one of the most common neurological complications observed in sepsis patients, contributing to both increased mortality and long-term cognitive impairment. Microglial mitochondrial reactive oxygen species (mtROS) overproduction and NLR family pyrin domain-containing 3 (NLRP3) inflammasome activation were key pathological drivers of SAE. Although PIM-1, a serine/threonine kinase, was known to regulate both mtROS generation and NLRP3 signaling, its specific contribution to SAE remained poorly defined.</div></div><div><h3>Methods</h3><div>This study established a SAE mouse model using cecal ligation and puncture (CLP) surgery, and screened the differentially expressed gene PIM-1 through immunohistochemistry, GEO database analysis, and etc. An <em>in vitro</em> model was established using Lipopolysaccharide + Adenosine(LPS + ATP) Triphosphate stimulated Mouse Microglia (BV-2), and the regulation mechanism of PIM-1 was analyzed through siRNA interference, RNA-seq, and etc. Potential drug Urolithin B (UB) targeting PIM-1 inhibition was screened through molecular docking, and its inhibitory effect on PIM-1 and therapeutic potential in SAE were evaluated through thermal stability experiments, behavioral experiments, etc.</div></div><div><h3>Results</h3><div>PIM-1 was upregulated in SAE, which was associated with brain damage. PIM-1 knockdown suppressed microglial activation and reduced inflammatory cytokines release. Further investigation indicated that PIM-1 modulated mtROS generation and facilitated NLRP3 inflammasome activation. Notably, pharmacological inhibition of PIM-1 by UB alleviated SAE both <em>in vivo</em> and <em>in vitro</em>, resulting in improved neuronal damage and cognitive impairment.</div></div><div><h3>Conclusion</h3><div>PIM-1 played a critical role in SAE progression, potentially through its mediation of microglial activation and neuroinflammation via the mtROS/NLRP3 axis. Notably, pharmacological inhibition of PIM-1 with urolithin B significantly alleviated SAE.</div></div>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":"241 ","pages":"Pages 469-487"},"PeriodicalIF":8.2,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145212098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exopolysaccharide from Lacticaseibacillus rhamnosus IR06 as a potential postbiotics attenuates photoaging through regulation of MAPK and NF-κB signaling.","authors":"Jin Hwan Kim, Won June Lee, Ka Young Choi, Sang-Ho Yoo, Seung Pil Pack, Nam Su Oh","doi":"10.1016/j.freeradbiomed.2025.09.053","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2025.09.053","url":null,"abstract":"<p><p>Exopolysaccharides (EPSs) are widely used in the food industry as stabilizers, viscosity enhancers, and thickeners due to their rheology-improving properties. Beyond food applications, EPSs have gained attention for their diverse biological effects, including antioxidant, anti-inflammatory, and anticancer activities. Ultraviolet B (UVB) radiation induces the production of intracellular reactive oxygen species (ROS), leading to skin damage such as epithelial barrier dysfunction, wrinkle formation, and inflammation. In this study, we investigated the protective effects of EPS derived from a potential probiotic lactic acid bacterium. The EPS from Lacticaseibacillus rhamnosus IR06 (EPS-IR06) exhibited notable in vitro protection against photoaging and inflammation. Characterization identified EPS-IR06 as a heteropolysaccharide with a glucose-branched galactomannan structure, with a molecular weight ranging from 3.9 × 10⁴ to 5.8 × 10⁵ Da. Treatment with EPS-IR06 on a UVB-induced 3D human skin model reduced epidermal damage and increased biomarkers associated with epidermal barrier function. Furthermore, EPS-IR06 effectively scavenged intracellular ROS and restored the balance of Nrf2-mediated antioxidant response in UVB-induced human epidermal keratinocytes. EPS-IR06 significantly reduced the expression of matrix metalloproteinases and pro-inflammatory mediators by modulating the MAPK and NF-κB signaling pathways. These findings suggest that EPS-IR06 could serve as a novel protective agent against UVB-induced skin damage, with potential applications in cosmetics and food industries.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145206105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Mesenchymal stromal cells deliver H₂S-enhanced Nrf2 via extracellular vesicles to mediate mitochondrial homeostasis for repairing hypoxia-ischemia brain damage\" [Free Radic. Biol. Med. 225 (2024) 528-545].","authors":"Chengcheng Gai, Tingting Li, Yijing Zhao, Yahong Cheng, Yan Song, Qian Luo, Dexiang Liu, Zhen Wang","doi":"10.1016/j.freeradbiomed.2025.09.048","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2025.09.048","url":null,"abstract":"","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}