Oxidative Medicine and Cellular Longevity最新文献

{"title":"Correction to \"Downregulated Recycling Process but Not De Novo Synthesis of Glutathione Limits Antioxidant Capacity of Erythrocytes in Hypoxia\".","authors":"","doi":"10.1155/omcl/9879523","DOIUrl":"10.1155/omcl/9879523","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9879523"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090152/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147717524","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":"Respirometry-Based Screening of Marine Natural Products Identifies Leptochelin A as a Novel Modulator of Mitochondrial Function.","authors":"Howard J Phang, Adrian M Arciniega, Jaclyn Bergstorm, Nicole E Avalon, Evgenia Glukhov, William H Gerwick, Anthony J A Molina","doi":"10.1155/omcl/9524037","DOIUrl":"10.1155/omcl/9524037","url":null,"abstract":"<p><p>While mitochondria are recognized as promising therapeutic targets for common pathologies of aging, existing drug discovery platforms fail to capture the adequate physiological and biological contexts necessary to identify translatable, clinically-relevant leads. The goal of this study was to identify marine natural products that modulate mitochondrial function using a screening pipeline leveraging primary human cells in a cell-based phenotypic primary screen. Using this approach, we identified leptochelin A, a recently described metallophore, as a candidate hit with strong potency and efficacy towards the inhibition of mitochondrial function. Using high-resolution respirometry and fluorescence imaging, we validated the mitochondrial-modulatory (\"mito-modulatory\") effects of leptochelin A and found that it inhibits multiple pathways in the electron transfer system (ETS) while having little effect on mitochondrial mass or superoxide production. It also increases mitochondrial ATP levels, though this may be attributable to a parallel increase in glycolysis. Our findings demonstrate the utility of phenotypic screening using human primary cells to identify novel mitochondrial modulators with translational potential. Leptochelin A's ability to inhibit mitochondrial function without imposing significant toxicity, coupled with its metal-chelating properties, make it a unique compound with therapeutic potential for aging and age-related disorders. Screening strategies focused on mitochondrial respiration can serve as a platform for the advancement of drug discovery within the pharmacology space of human aging.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9524037"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13213193/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148033869","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 \"Rh-CXCL-12 Attenuates Neuronal Pyroptosis after Subarachnoid Hemorrhage in Rats via Regulating the CXCR4/NLRP1 Pathway\".","authors":"","doi":"10.1155/omcl/9756127","DOIUrl":"10.1155/omcl/9756127","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9756127"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147513686","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":"FUNDC1-Associated Regulation of Mitochondrial Function Is Crucial for Preventing Endothelial Injury in Hyperglycemia.","authors":"Vinothkumar Rethineswaran, Young Joon Hong, Woong Bi Jang, Jaewoo Choi, Hye Ji Lim, Sangmi Park, Eun Ji Lee, Jong Seong Ha, Jisoo Yun, Sang-Mo Kwon","doi":"10.1155/omcl/6619225","DOIUrl":"10.1155/omcl/6619225","url":null,"abstract":"<p><p>Mitochondria are intracellular organelles that regulate cell survival and death. Hyperglycemia modulates the functioning of the mitochondria in endothelial cells. We discovered that high-glucose (HG) treatment reduces FUN14 domain-containing 1 (FUNDC1) expression in endothelial cells. FUNDC1 expression in the mitochondria inhibits the proteasomal degradation of cytochrome C oxidase IV (COX-IV) and regulates mitochondrial complex I and IV activities as well as ATP synthesis under normal conditions. The FUNDC1 depletion in HG contexts affects mitochondrial complex I and IV activity as well as ATP synthesis and promotes mitochondrial damage through the loss of mitochondrial membrane potential and the production of reactive oxygen species (ROS). BAM15 is a mitochondrial uncoupler that increases mitochondrial function and endothelial survival. Cotreatment with HG and BAM15 increased the FUNDC1 protein expression level and the mitochondrial translocation of FUNDC1 in HG-treated cells. The BAM15-induced upregulation of FUNDC1 expression increased the mitochondrial expression of COX-IV, complex I and IV activity, and ATP synthesis. Our findings suggest that FUNDC1 expression in endothelial cells under hyperglycemic stress plays a crucial role in limiting vascular damage and apoptotic cell death. We discovered a mechanism through which BAM15 protects endothelial cells through FUNDC1-mediated mitophagy and metabolic regulation. Targeting FUNDC1 via mitochondrial uncoupling is a promising therapeutic strategy for treating diabetic vascular diseases.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e6619225"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13250841/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148212151","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":"Modelling Ferroptosis in a Human Microglial Line by Sequential Exposure to Iron and GPX4 Inhibition.","authors":"Renaud Bussiere, Nikhil Tulsian, Cecilia Wieder, Dewi McConnaughie, Evie Tynan, Andrew Lowe, Esther Cheow, Matthew Choo, Jill C Richardson, James A Duce, Sébastien Gillotin","doi":"10.1155/omcl/9948225","DOIUrl":"10.1155/omcl/9948225","url":null,"abstract":"<p><p>Excessive iron accumulation is a pathological feature of several neurodegenerative diseases (NDDs), and a growing body of evidence suggests that ferroptosis, an iron-dependent form of regulated cell death (RCD) driven by lipid peroxidation, is implicated in their pathogenesis. Microglia, the brain's resident immune cells, buffer iron overload but become susceptible to ferroptotic death, exacerbating neuroinflammation and neuronal loss. To uncover the molecular events leading to microglial ferroptosis, we established a human microglial ferroptosis model using the HMC3 cell line. This model recapitulates core features of ferroptosis, including increased reactive oxygen species (ROS) and peroxidation of lipids at the membrane, both rescued by ferrostatin-1 (Fer-1). We used this model to perform integrated multiomic profiling and identified significant dysregulation in lipid species, notably an accumulation of sterols, including oxysterols such as 7-oxo-cholesterol, alongside the oxidation of polyunsaturated fatty acids (PUFAs) that are characteristic of ferroptosis. Transcriptomic and proteomic analyses corroborate these findings, revealing the upregulation of the mevalonate pathway and cholesterol metabolism. Importantly, the increased expression of some of these key metabolic genes was also reversed by Fer-1 treatment, indicating their role in a preferroptotic signature. Our model provides a novel platform for investigating early molecular events in microglia ferroptosis. Integrating these findings into future investigations could uncover new protective mechanisms against microglial ferroptosis to ensure homeostatic regulation of ROS levels and sterol metabolism.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9948225"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13463428/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148713418","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":"RETRACTION: Internalization of Staphylococcus aureus in Lymphocytes Induces Oxidative Stress and DNA Fragmentation: Possible Ameliorative Role of Nanoconjugated Vancomycin.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9803095","DOIUrl":"10.1155/omcl/9803095","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9803095"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13371086/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148448642","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 \"Chronic Cerebral Hypoperfusion Aggravates Parkinson's Disease Dementia-Like Symptoms and Pathology in 6-OHDA-Lesioned Rat through Interfering with Sphingolipid Metabolism\".","authors":"","doi":"10.1155/omcl/9801758","DOIUrl":"10.1155/omcl/9801758","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9801758"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13051818/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147623442","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":"RETRACTION: Elevated Glutathione Peroxidase 2 Expression Promotes Cisplatin Resistance in Lung Adenocarcinoma.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9757854","DOIUrl":"10.1155/omcl/9757854","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9757854"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140426/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147581917","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":"RETRACTION: Activation of AdipoR1 with rCTRP9 Preserves BBB Integrity through the APPL1/AMPK/Nrf2 Signaling Pathway in ICH Mice.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9852076","DOIUrl":"10.1155/omcl/9852076","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9852076"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140242/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147468787","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 Neonatal Disease: Established Organ Injury and Emerging Evidence for Skeletal Involvement.","authors":"Laura Cannavò, Virginia Beretta, Chiara Petrolini, Vincenzo Raitano, Elena Scarpa, Valentina Dell'Orto, Silvia Carloni, Maria Cristina Albertini, Serafina Perrone","doi":"10.1155/omcl/8655644","DOIUrl":"10.1155/omcl/8655644","url":null,"abstract":"<p><p>Reactive oxygen and nitrogen species participate in physiological signaling and adaptation during fetal and neonatal development, whereas excessive, prolonged, or spatially dysregulated production may contribute to oxidative and nitrosative tissue injury. Redox dysregulation has been extensively investigated in neonatal conditions, including bronchopulmonary dysplasia (BPD), hypoxic-ischemic encephalopathy, retinopathy of prematurity (ROP), necrotizing enterocolitis (NEC), congenital heart disease (CHD), and hyperbilirubinemia. Its relationship with bone metabolism is well established in adult and pediatric disorders, including osteoporosis, inflammatory bone loss, and iron-overload-related bone disease. However, the potential contribution of perinatal redox imbalance to early skeletal development remains comparatively underexplored. This narrative review critically examines the biochemical mechanisms of reactive species generation, their interaction with inflammatory pathways, and the experimental and clinical evidence linking redox dysregulation to neonatal organ injury. Particular attention is given to the developing skeleton as a potentially underrecognized target. Experimental studies indicate that excessive reactive species can impair chondrogenesis, alter osteoblast and osteoclast activity, disrupt collagen and osteogenic signaling, and interfere with skeletal growth. Human evidence is predominantly observational. Preliminary longitudinal data show inverse associations between cord-blood markers of oxidative DNA and protein modification and REMS-derived skeletal Z-scores during the first year of life. These findings suggest that early redox imbalance may impair bone quality and growth trajectories in newborns. Prospective studies integrating standardized redox biomarkers, bone-metabolism indices, imaging, nutrition, medication exposure, growth, and fracture outcomes are needed to determine whether redox dysregulation independently contributes to impaired skeletal development.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e8655644"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149148209","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}