Oxidative Medicine and Cellular Longevity最新文献

{"title":"Ebselen: A Multifaceted Organoselenium Compound With Therapeutic Potential in Liver Diseases.","authors":"Lujain Bader Eddin, Shreesh Ojha","doi":"10.1155/omcl/9370771","DOIUrl":"10.1155/omcl/9370771","url":null,"abstract":"<p><p>Both oxidative stress and inflammation are considered the driving mechanisms in most liver pathologies. Therefore, identifying pharmacological compounds with antioxidant and anti-inflammatory properties is central to curbing hepatic diseases. Ebselen is a synthetic organoselenium compound with glutathione peroxidase (GPx)-like activity, demonstrating potent antioxidant and anti-inflammatory effects experimentally. Ebselen targets several molecular mechanisms involved in hepatic cellular injury. It maintains redox-sensitive signaling, neutralizes reactive free radicals, and regulates thiol-dependent enzymes in experimental models of drug-induced, ischemia-reperfusion, and metabolic liver diseases. Studies provided experimental evidence for Ebselen's role in suppressing lipid peroxidation, preserving mitochondrial dynamics, inhibiting inflammatory response, and protecting hepatocytes in cell lines as well as murine models of different liver injuries. Findings also reported an indirect effect on cellular demise and fibrogenesis through inhibiting the activation of hepatic stellate cells (HSCs) and decreasing collagen deposition. The hepatoprotective effects of Ebselen also extend to include reducing hepatic lipid accumulation and preventing steatosis induction in rodent models of liver fibrosis. This review summarizes the current available evidence on the hepatoprotective effects of Ebselen.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9370771"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527384/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148866278","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":"EXPRESSION OF CONCERN: Neuroprotective Effect of Tea Polyphenols on Oxyhemoglobin Induced Subarachnoid Hemorrhage in Mice.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9848436","DOIUrl":"10.1155/omcl/9848436","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9848436"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147499576","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":"Interplay of Mitochondrial Dynamics, Nutrition, and Vitamins: Evidence From Experimental and Human Studies With Implications for Women's Health.","authors":"Kunjal Kiran Pai, Shambhavi Shetye, Rakshith Patil, Shravya Acharya, Kishan S Kulal, Ajeetkumar Patil, Saritha U Kamath","doi":"10.1155/omcl/8685788","DOIUrl":"10.1155/omcl/8685788","url":null,"abstract":"<p><strong>Background: </strong>Nutrition is a key modifiable factor supporting mitochondrial health and is essential for ovarian function and women's health across the life course. From menarche to menopause, mitochondrial efficiency underpins physiological balance. The menopausal transition is particularly critical, as hormonal and neuroendocrine changes are associated with impaired mitochondrial function and increased risk of age-related disorders.</p><p><strong>Aim: </strong>This review aimed to systematically review and synthesize the available evidence on mitochondrial function across in vitro, animal, and human studies and to evaluate the potential protective role of vitamins and nutrients in maintaining mitochondrial health, with attention to sex-specific findings.</p><p><strong>Methods: </strong>A systematic search was conducted across multiple electronic databases. Forty-six eligible studies were identified and critically reviewed for evidence on mitochondrial function, sex-based differences, and nutritional influences.</p><p><strong>Results: </strong>Mitochondrial dysfunction may contribute to the pathophysiology of age-related disorders, including osteoporosis, cardiovascular disease, neurodegenerative conditions, and cancer. Nutritional factors are crucial for preserving mitochondrial integrity. Vitamins C, E, and D, NAD + precursors such as nicotinamide riboside, coenzyme Q10, MitoQ, fucoxanthin, and cabergoline reduce oxidative stress, enhance mitochondrial biogenesis, support electron transport chain activity and ATP production, and maintain redox balance. These actions promote mitochondrial resilience and cellular energy metabolism. Evidence further indicates that women, particularly during the menopausal transition, exhibit heightened vulnerability to mitochondrial dysfunction, highlighting the relevance of nutrition-based interventions.</p><p><strong>Conclusion: </strong>Optimizing dietary intake of vitamins, antioxidants, and mitochondrial cofactors is a cost-effective, accessible strategy to support mitochondrial health and reduce age-related disease risk in women.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e8685788"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13305678/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148331921","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":"Experimental and In Silico Evaluation of Honey-Derived Phenolic Compounds: Antioxidant Activity, Anti-Inflammatory Potential Pharmacokinetic Properties, Toxicity Assessment, and Multitarget Anti-Inflammatory Potential.","authors":"Eda Sonmez Gurer, Sevgi Durna Dastan, Zeliha Selamoglu, Ainash Oshibayeva, Taner Dastan, Nurdana Salybekova","doi":"10.1155/omcl/6342617","DOIUrl":"10.1155/omcl/6342617","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Honey is a natural product rich in phenolic compounds that contribute to its antioxidant and anti-inflammatory properties. The present study aimed to evaluate the biological activities of honey samples collected from different regions of Kazakhstan through experimental assays and computational analyses of major honey-derived phenolic compounds. Ethanolic extracts of seven honey samples were prepared and assessed for extraction yield, total phenolic content, total flavonoid content (TFC), antioxidant activity using the DPPH radical scavenging assay, and anti-inflammatory activity using the albumin denaturation inhibition assay. In addition, five representative honey-derived phenolic compounds, namely fumaric acid, p-hydroxybenzoic acid, p-coumaric acid, trans-2-hydroxycinnamic acid, and chrysin, were subjected to comprehensive in silico analyses including ADME prediction, drug-likeness evaluation, toxicity assessment, and multitarget molecular docking. Extraction yields ranged from 6.8% to 8.7%. The highest total phenolic content was observed in sample B12 (80.1 ± 9.7 mg GAE/g extract), whereas the highest TFC was detected in sample B10 (6.8 ± 0.5 mg quercetin equivalent (QE)/g extract). DPPH radical scavenging activity revealed IC&lt;sub&gt;50&lt;/sub&gt; values ranging from 2.5 ± 0.1 to 5.6 ± 0.4 mg/mL, with samples B11, B12, and B10 exhibiting the strongest antioxidant activities. In the albumin denaturation assay, all extracts demonstrated concentration-dependent anti-inflammatory activity, with inhibition percentages reaching 33.9% ± 2.0% at 100 mg/mL. The ADME analysis revealed that all investigated compounds exhibited favorable drug-likeness properties and high predicted gastrointestinal (GI) absorption. Chrysin demonstrated the highest lipophilicity and receptor-binding potential, whereas p-coumaric acid and trans-2-hydroxycinnamic acid showed the most balanced pharmacokinetic profiles. Toxicity predictions performed using ProTox-3.0, pkCSM, and admetSAR indicated low risks of hepatotoxicity and nephrotoxicity, with no predicted neurotoxicity, respiratory toxicity, carcinogenicity, or mutagenicity for any of the compounds. Molecular docking analyses against multiple inflammation-related targets, including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), nuclear factor kappa-B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and protein kinase B (AKT1), demonstrated strong binding affinities, particularly for trans-2-hydroxycinnamic acid and chrysin. These compounds exhibited favorable interactions with several key mediators of inflammatory signaling, suggesting potential multitarget mechanisms of action. Computational analyses demonstrated favorable drug-likeness characteristics and high predicted GI absorption for all investigated compounds. Toxicity predictions indicated low risks of hepatotoxicity and nephrotoxicity, with no predicted neurotoxicity, respiratory toxicity, carcinogenicity, or mutagenicity. Mo","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e6342617"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13532570/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148866270","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":"Oxidative Stress in Heat Stress Nephropathy: Crosstalk.","authors":"Justice Afrifa, Eric Gyamerah Ofori, Evans Duah, Ibrahim W Naveh-Fio, Gabriel Pezahso Kotam, Yeboah Kwaku Opoku, Addae Boateng Adu-Gyamfi, Helena Acquah, Enoch Essiam, Samuel Essien-Baidoo, Kwame Kumi Asare, Richard K D Ephraim","doi":"10.1155/omcl/1708417","DOIUrl":"10.1155/omcl/1708417","url":null,"abstract":"<p><p>Heat stress (HS) is a growing public health concern as rising global temperatures and occupational hazards expose a significant portion of the world's population to extreme heat. The kidneys are particularly vulnerable to heat-induced injuries, with oxidative stress (OS) playing a central role in their pathogenesis. The process involves heat-induced mitochondrial dysfunction and stimulation of inflammatory pathways. This leads to the production of excessive reactive oxygen species (ROS) that eventually overwhelm the kidney's natural antioxidant defenses. The resultant OS directly damages lipids, proteins, and DNA in renal tubular cells, a condition that is worsened by systemic inflammation and renal hypoxia. Although cells initially activate protective mechanisms involving heat shock proteins (HSPs) to preserve mitochondrial integrity, prolonged heat exposure undermines these defenses, increasing stress and triggering apoptotic pathways. This article focuses on the impact of HS on kidney health and the role of OS in the pathogenesis of heat-induced kidney injuries. Key markers of heat-induced OS, such as lipid peroxidation products (e.g., malondialdehyde [MDA], F₂-isoprostanes, 4-hydroxynonenal [4-HNE], and 8-hydroxy-2'-deoxyguanosine [8-OHdG]) and their effects on hematological indices and inflammatory response are highlighted. Ultimately, clarifying these specific mechanisms is essential to guide the development of early diagnostic tools and targeted treatments. This will help to reduce kidney damage, especially in vulnerable populations. We suggest that strategies such as adequate hydration, educating vulnerable groups on signs of heat strain, wearing light clothing, and heat acclimatization can mitigate the adverse effects of the rising global temperatures on kidney health.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e1708417"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13392506/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148562592","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":"Expression of Concern: \"SIRT1 Activation by Resveratrol Alleviates Cardiac Dysfunction via Mitochondrial Regulation in Diabetic Cardiomyopathy Mice\".","authors":"","doi":"10.1155/omcl/9834761","DOIUrl":"10.1155/omcl/9834761","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9834761"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13618926/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149075649","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":"Skin Aging and Mitochondrial Dysfunction: Structural Changes, Mechanistic Insights, and Therapeutic Perspectives.","authors":"Nathália Cardoso de Afonso Bonotto, Elize Musachio, Giulliano Danezi Felin, Giancarllo Danezi Felin, Carla Helena Augustin Schwanke, Ivana Beatrice Mânica da Cruz, Fernanda Barbisan","doi":"10.1155/omcl/5140711","DOIUrl":"10.1155/omcl/5140711","url":null,"abstract":"<p><p>This narrative review discusses the relationship between structural changes in the skin and mitochondrial function during aging and evaluates emerging therapeutic interventions targeting mitochondrial dysfunction. An analysis of 49 scientific articles published between 2015 and 2025 was conducted using descriptors including \"skin aging,\" \"mitochondrial dysfunction,\" \"oxidative stress,\" and \"cutaneous senescence,\" and articles were retrieved from PubMed, Scopus, and ScienceDirect. Additional research was conducted using terms related to therapeutic interventions, including \"mitochondrial therapies AND skin aging OR cutaneous aging.\" Original research articles were included based on thematic relevance, recency, and scientific rigor. The reviewed studies suggest that oxidative stress, mainly from mitochondrial metabolism, is a primary cause of skin cell senescence. Mitochondrial dysfunction emerges as a central mechanistic hub linking oxidative stress, mitochondrial genome instability, chronic low-grade inflammation (inflammaging), and the senescence-associated secretory phenotype (SASP) to age-related structural and functional skin alterations. Mitochondria maintain skin homeostasis through cell proliferation, differentiation, and genetic material synthesis. With advancing age, mitochondrial DNA copy number declines significantly, while reactive oxygen species production increases, thereby compromising cellular energy metabolism. Emerging mitochondrial-targeted therapeutic strategies, including nicotinamide adenine dinucleotide (NAD⁺) precursors, coenzyme Q10 supplementation, senolytics, and modulators of mitochondrial quality control, show promising effects on skin aging parameters in preclinical and early clinical studies. However, current evidence is based on small clinical trials with short follow-up periods, and long-term safety data remain limited. Therefore, while mitochondria are not the sole source of oxidants, growing evidence indicates that oxidative stress-driven mitochondrial dysfunction represents a priority pathogenic mechanism in skin aging. The clinical translation of mitochondrial-targeted therapies represents an innovative opportunity for anti-aging strategies, although the validation of standardized biomarkers and longitudinal safety investigations remains critical for clinical implementation.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e5140711"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13175270/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147942343","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":"Integrated Analysis of Pithecellobium dulce Leaf Fractions for Ex Vivo Antioxidant, DNA Damage Protective, and Afzelin-Mediated Anti-Inflammatory Potentials via In Vivo and In Silico Approaches.","authors":"Masuma Akter, Mst Shahnaj Parvin, Md Ekramul Islam","doi":"10.1155/omcl/5529212","DOIUrl":"10.1155/omcl/5529212","url":null,"abstract":"<p><p>As medicinal plants offer promising alternatives to synthetic drugs, this study explored the ex vivo antioxidant and in vitro anti-inflammatory capacities of Pithecellobium dulce leaf extracts, alongside the in vivo anti-inflammatory potential of its bioactive flavonoid, afzelin, using experimental and computational approaches. In erythrocytes, 2,2^'-azobis(2-amidinopropane)dihydrochloride (AAPH) induced a time-dependent increase in hemolysis, malondialdehyde (MDA) formation, and depletion of cytosolic glutathione (GSH) and superoxide dismutase (SOD). The chloroform fraction (CHF) and ethyl acetate fraction (EAF) mitigated hemolysis and lipid peroxidation, enhanced GSH and SOD levels, lowered MDA levels compared with the AAPH group, and also protected P^UC19 plasmid DNA from oxidative damage. In anti-inflammatory assays, EAF and CHF inhibited heat-induced red blood cell (RBC) lysis by 57.31% ± 0.80% and 51.39% ± 0.27% and egg albumin denaturation by 39.74% ± 0.77% and 37.20% ± 2.16%, respectively, compared with 61.52% ± 0.58% for acetylsalicylic acid. Afzelin (50 mg/kg body weight) reduced carrageenan-induced paw edema by 56.16%, versus 70.83% for diclofenac sodium. Bioinformatics analysis identified 38 potential anti-inflammatory protein targets of afzelin, of which 11 were further examined via molecular docking. Docking results revealed favorable binding energies for all targets, with the highest affinity observed for JAK3 (-9.60 kcal/mol) compared to native ligands. These computational results suggest that afzelin can form stable, energetically favorable interactions with multiple key proinflammatory proteins. Overall, these findings indicate that P. dulce leaf extracts possess significant antioxidant and anti-inflammatory activities, and afzelin showed predicted interactions with multiple kinase and nonkinase inflammation-associated proteins.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e5529212"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13680805/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224687","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":"Ginsenoside Rb1 Improves Atherosclerosis by Inhibiting Endothelial Cell Pyroptosis.","authors":"Xuejiao Jiang, Tianqi Jiang, Zhaoyu Pan, Chun Chen, Xinyu Ji, Xiongyao Wang, Wenjing Zong","doi":"10.1155/omcl/6137635","DOIUrl":"10.1155/omcl/6137635","url":null,"abstract":"<p><strong>Purpose: </strong>This study aimed to investigate the effect of ginsenoside Rb1 (Gs-Rb1) on endothelial cell (EC) pyroptosis in atherosclerosis (AS).</p><p><strong>Method: </strong>ApoE^-/- mice and mouse aortic endothelial cells (MAECs) were used as research subjects. An in vivo AS model was established by feeding ApoE^-/- mice a high-fat diet (HFD) for 3 months, followed by intragastric administration of Gs-Rb1 at 40 mg/kg/day for 3 months. Pathological changes were evaluated by hematoxylin-eosin (HE) and Oil Red O staining. Caspase-1 expression was detected by immunofluorescence. Pyroptosis-related protein and mRNA levels were measured by Western blotting and RT-PCR. Inflammatory factors (IL-18 and IL-1β) and LDH were quantified by ELISA. For in vitro experiments, MAECs were stimulated with oxidized low-density lipoprotein (ox-LDL, 150 μg/mL) to induce pyroptosis, followed by treatment with Gs-Rb1 (60 or 80 μg/mL) for 12 h. Cell death was assessed by flow cytometry.</p><p><strong>Result: </strong>Gs-Rb1 significantly reduced aortic plaque area in mice. It decreased the expression of pyroptosis-related proteins (caspase-1, cleaved caspase-1, GSDMD, and NLRP3) and mRNA levels in aortic tissues. Serum levels of LDH, IL-18, and IL-1β were also significantly reduced. In vitro, Gs-Rb1 reduced cell death rate and inhibited pyroptosis in endothelial cells (ECs).</p><p><strong>Conclusion: </strong>This study confirms the therapeutic effect of Gs-Rb1 on AS at both animal and cellular levels. Inhibition of EC pyroptosis may be the key mechanism underlying the anti-atherosclerotic effects of Gs-Rb1.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e6137635"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13129223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777889","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":"Correction to \"Identification of Resolvin D1 and Protectin D1 as Potential Therapeutic Agents for Treating Kidney Stones\".","authors":"","doi":"10.1155/omcl/9857091","DOIUrl":"10.1155/omcl/9857091","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9857091"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13067053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147646054","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}