Oxidative Medicine and Cellular Longevity最新文献

{"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}

{"title":"Intermittent Fasting Potentiates Aerobic Exercise to Reduce Hippocampal Amyloid Burden and Oxidative Stress via Suppression of NF-κB/NLRP3 Signaling in an Aβ-Injected Rat Model.","authors":"Taner Atasoy, Heidar Sajedi, Davar Khodadadi, Burak Tozoğlu, Mehmet Şirin Güler, Serkan Tevabil Aka, Mohammad Babaei","doi":"10.1155/omcl/9921337","DOIUrl":"10.1155/omcl/9921337","url":null,"abstract":"<p><p>NOD-like receptor protein 3 (NLRP3) inflammasome-driven neuroinflammation contributes to Alzheimer's disease (AD) progression, yet effective strategies to target this pathway are limited. We investigated whether aerobic exercise performed in a fasted state, rather than the fed state, would potentiate β-hydroxybutyrate (BHB)-dependent inhibition of NLRP3 inflammasome signaling. Twenty-month-old male Wistar rats were randomly assigned to five groups: AD, AD + intermittent fasting (ADIF), AD + aerobic exercise (ADAE), ADIF + aerobic exercise (ADIFAE), and sham-injected control (SC). AD-like pathology was induced by bilateral intrahippocampal injection of amyloid-β (Aβ)_1-42. The IF regimen consisted of a daily 14-h fast (06:00-20:00). Exercise consisted of moderate-intensity treadmill running (5 days/week for 4 weeks), either in the fed state or after ∼12.5 h of fasting. Aβ injection impaired spatial learning and memory, elevated soluble Aβ_1-42 (sAβ), malondialdehyde (MDA), NF-κB, NLRP3, caspase-1, interleukin-1β (IL-1β), and IL-18, and reduced superoxide dismutase (SOD) activity and brain-derived neurotrophic factor (BDNF) expression in the hippocampus (p  < 0.05). Both IF and exercise partially reversed cognitive impairments by reducing sAβ and oxidative stress, increasing BHB, suppressing NF-κB/NLRP3 signaling, and restoring BDNF (p  < 0.05), while fasted-state exercise produced significantly larger effects than either intervention alone (p  < 0.05). Our findings suggest that performing exercise in a fasted state provides complementary metabolic, anti-inflammatory, and cognitive benefits that exceed those of either intervention alone. This combined regimen may represent a promising nonpharmacological strategy for targeting metabolic-immune and neurotrophic pathways relevant to AD progression.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9921337"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13184385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147974359","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: Computational and Preclinical Evidence of Anti-ischemic Properties of L-Carnitine-Rich Supplement via Stimulation of Anti-inflammatory and Antioxidant Events in Testicular Torsed Rats.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9793178","DOIUrl":"10.1155/omcl/9793178","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9793178"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13352352/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148422931","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 \"Oxidative and Inflammatory Mechanisms Induced by Intermittent Hypoxia Leading to Vascular Alterations in Rodents: A Systematic Review and Meta-Analysis\".","authors":"","doi":"10.1155/omcl/9854762","DOIUrl":"10.1155/omcl/9854762","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9854762"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13058812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147634070","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: Preparation and Multitarget Anti-AD Activity Study of Chondroitin Sulfate Lithium in AD Mice Induced by Combination of D-Gal/AlCl₃.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9763163","DOIUrl":"10.1155/omcl/9763163","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9763163"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147468866","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: Dietary Supplementation of the Antioxidant Curcumin Halts Systemic LPS-Induced Neuroinflammation-Associated Neurodegeneration and Memory/Synaptic Impairment via the JNK/NF-κB/Akt Signaling Pathway in Adult Rats.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9837507","DOIUrl":"10.1155/omcl/9837507","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9837507"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13288252/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148302621","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: NPC-EXs Alleviate Endothelial Oxidative Stress and Dysfunction through the miR-210 Downstream Nox2 and VEGFR2 Pathways.","authors":"","doi":"10.1155/omcl/9891762","DOIUrl":"10.1155/omcl/9891762","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9891762"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13352354/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148422936","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":"New Insight Into Male Infertility: Deviation From Basic Tenets of Life.","authors":"Mohammad Hossein Nasr-Esfahani, Nushin Naderi, Marziyeh Tavalaee, Mazdak Razi","doi":"10.1155/omcl/4433444","DOIUrl":"10.1155/omcl/4433444","url":null,"abstract":"<p><p>Male reproductive health faces mounting concern as global sperm concentration (SC) has declined markedly, with evidence linking this trend to environmental and lifestyle factors rather than natural variability. In parallel, rising rates of obesity, diabetes, and hypertension point to shared mechanisms with infertility, particularly those rooted in diet. High intake of processed sugars, especially high-fructose corn syrup (HFCS), contributes to metabolic dysfunction, oxidative stress, hormonal imbalance, and inflammation, all of which can impair sperm function and disrupt the hypothalamic-pituitary-gonadal (HPG) axis. Unlike glucose, fructose undergoes hepatic metabolism, fostering insulin resistance, fat accumulation, and nonalcoholic fatty liver disease (NAFLD), further aggravating reproductive risks. In this review, four models of obesity, the energy balance model (EBM), carbohydrate-insulin model (CIM), obesogen model, and OBS/REDOX model, are applied to explain how excess fructose and obesogenic exposures drive metabolic dysfunction, oxidative stress, and endocrine disruption. Collectively, these processes reduce testosterone levels, impair spermatogenesis, compromise sperm quality, and may even induce epigenetic alterations transmissible to future generations. With modern diets increasingly dominated by HFCS and ultra-processed foods (UPFs), understanding fructose's role in reproductive decline is crucial for developing effective interventions. This review underscores the need for further research to clarify how dietary fructose and environmental obesogens jointly shape metabolic and reproductive health, offering insights into public health strategies aimed at protecting male fertility in the face of modern lifestyle challenges.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e4433444"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148866344","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":"Prolonged Oxidative Stress Drives p53/p21-Mediated Senescence and Degenerative Adaptation in Kidney-Derived Cells.","authors":"Napat Armartmuntree, Waleeporn Kaewlert, Paweeticha Aupatham, Supansa Buakaew, Chadamas Sakonsinsiri, Worachart Lert-Itthiporn, Somchai Pinlaor, Raynoo Thanan","doi":"10.1155/omcl/3094707","DOIUrl":"10.1155/omcl/3094707","url":null,"abstract":"<p><p>Chronic oxidative stress has long been implicated in renal pathologies, but whether sustained oxidative damage primarily promotes chronic kidney disease (CKD) or tumorigenesis remains unclear. To address this question, we investigated the long-term effects of oxidative stress on human embryonic kidney (HEK293T) cells chronically exposed to a low dose of hydrogen peroxide (H₂O₂, 50 μM H₂O₂) for 9 months, generating two adapted lines, 50R30 and 50R45. These cells exhibited enhanced survival and tolerance to acute high-dose H₂O₂ challenge, indicating an oxidative stress-resistant phenotype. Despite this adaptation, both cell lines showed markedly reduced proliferation and migration, reflecting loss of cellular vitality and function typical of renal degeneration. Transcriptomic and protein analyses revealed upregulation of genes and proteins involved in cell-cycle arrest (p53 and p21), senescence, and the NF-κB/IL-6-driven senescence-associated secretory phenotype (SASP), oxidative stress responses, together with elevated heat shock factor 1 (HSF1) expression indicative of biomolecular damage and impaired adaptive capacity. Collectively, these findings suggest that chronic oxidative stress drives cellular aging and dysfunction rather than malignant transformation, leading to degenerative changes resembling CKD pathology. Moreover, prolonged oxidative stress alone appears insufficient to induce carcinogenic transformation; additional genetic or epigenetic alterations, together with specific cellular machinery, are likely required to drive kidney malignancy. This study therefore provides mechanistic insight into how sustained oxidative stress promotes renal cell senescence and contributes to CKD progression.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e3094707"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13450133/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685552","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 Lipid Line of Defence: Monounsaturated Fatty Acids (MUFAs) in Cancer and Ferroptosis.","authors":"Sneha D Baadkar, Amoolya Kandettu, Swagat Ray, Sanjiban Chakrabarty","doi":"10.1155/omcl/9604592","DOIUrl":"https://doi.org/10.1155/omcl/9604592","url":null,"abstract":"<p><strong>Background: </strong>Monounsaturated fatty acid (MUFA) metabolism promotes cancer progression and survival by regulating membrane lipid composition, maintaining lipid homeostasis and preserving redox balance. A growing body of evidence indicates that altered MUFA metabolism promotes tumour growth while protecting cancer cells from ferroptosis.</p><p><strong>Aim: </strong>This review summarises current knowledge on the contributions of MUFA metabolism to carcinogenesis, regulation of ferroptosis and treatment response across different cancers. Further, we discussed the emerging treatment strategies targeting MUFA metabolic pathways.</p><p><strong>Methods: </strong>Relevant experimental and clinical studies investigating MUFA metabolism, lipid metabolic reprogramming, ferroptosis and therapeutic interventions in cancer were comprehensively reviewed and critically analysed.</p><p><strong>Results: </strong>Enhanced de novo MUFA synthesis and incorporation into membrane phospholipids increase the MUFA-to-polyunsaturated fatty acid (PUFA) ratio, thereby reducing the availability of oxidation-prone PUFAs, limiting lipid peroxidation, and protecting cancer cells from ferroptosis. MUFA-driven membrane remodelling enhances membrane fluidity and activates oncogenic signalling pathways, including epithelial-mesenchymal transition (EMT), cancer cell migration, invasion and metastasis. These effects are mediated by the dysregulated expression of key lipogenic enzymes and signalling pathways that reprogramme lipid metabolism to meet the metabolic demands of cancer cells. Multiple studies have shown that MUFA metabolism is a promising therapeutic target. Furthermore, the inhibition of stearoyl-CoA desaturase-1 (SCD1) and fatty acid synthase (FASN), key enzymes in MUFA metabolism, sensitises cancer cells to ferroptosis by enhancing lipid peroxidation.</p><p><strong>Conclusion: </strong>MUFA metabolism is a key regulator of cancer progression and ferroptosis resistance. Targeting MUFA metabolic pathways is a promising therapeutic strategy. However, mechanistic studies are required to elucidate the molecular mechanisms underlying sensitivity to ferroptosis and to optimise clinical applications.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9604592"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13659645/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183854","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}