Oxidative Medicine and Cellular Longevity最新文献

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Correction to "The Combination of Individual Herb of Mi-Jian-Chang-Pu Formula Exerts a Synergistic Effect in the Treatment of Ischemic Stroke in Rats". 修正“米健肠普方单方联合对缺血性脑卒中大鼠有增效作用”。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-01 DOI: 10.1155/omcl/9795781
{"title":"Correction to \"The Combination of Individual Herb of Mi-Jian-Chang-Pu Formula Exerts a Synergistic Effect in the Treatment of Ischemic Stroke in Rats\".","authors":"","doi":"10.1155/omcl/9795781","DOIUrl":"10.1155/omcl/9795781","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9795781"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140233/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147459383","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}
引用次数: 0
EXPRESSION OF CONCERN: Effect of Chronic Administration of Resveratrol on Cognitive Performance during Aging Process in Rats. 关注表达:长期服用白藜芦醇对大鼠衰老过程中认知能力的影响。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-01 DOI: 10.1155/omcl/9807402
Oxidative Medicine And Cellular Longevity
{"title":"EXPRESSION OF CONCERN: Effect of Chronic Administration of Resveratrol on Cognitive Performance during Aging Process in Rats.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9807402","DOIUrl":"10.1155/omcl/9807402","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9807402"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147513689","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}
引用次数: 0
RETRACTION: Exosomes Released from CaSR-Stimulated PMNs Reduce Ischaemia/Reperfusion Injury. 收缩:从casr刺激的PMNs释放的外泌体减少缺血/再灌注损伤。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-01 DOI: 10.1155/omcl/9769386
Oxidative Medicine And Cellular Longevity
{"title":"RETRACTION: Exosomes Released from CaSR-Stimulated PMNs Reduce Ischaemia/Reperfusion Injury.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9769386","DOIUrl":"10.1155/omcl/9769386","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9769386"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13100975/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777906","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}
引用次数: 0
Crosstalk Between the NRF2 Signaling Pathway and Heat Shock Proteins: Implications for Cellular Stress Response and Disease Therapy. NRF2信号通路和热休克蛋白之间的串扰:对细胞应激反应和疾病治疗的影响。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-01 DOI: 10.1155/omcl/8809922
Milad Faraji, Saeed Nazifi
{"title":"Crosstalk Between the NRF2 Signaling Pathway and Heat Shock Proteins: Implications for Cellular Stress Response and Disease Therapy.","authors":"Milad Faraji, Saeed Nazifi","doi":"10.1155/omcl/8809922","DOIUrl":"10.1155/omcl/8809922","url":null,"abstract":"<p><p>Cells are continuously exposed to oxidative and proteotoxic stress that disrupt redox balance and protein homeostasis. Two major cytoprotective systems-the nuclear factor erythroid 2-related factor 2 (NRF2) pathway and the heat shock response (HSR) mediated by heat shock factor 1 (HSF1) and heat shock proteins (HSPs)-form an interconnected stress-adaptation network that coordinates redox defense, proteostasis, and cellular survival. Although historically viewed as largely independent pathways, accumulating evidence demonstrates extensive bidirectional and context-dependent crosstalk through transcriptional coregulation, protein-protein interactions, posttranslational mechanisms, and shared molecular hubs, including p62/SQSTM1 and the ubiquitin-proteasome system. This network integrates antioxidant defense with protein quality control, mitochondrial homeostasis, and inflammatory and metabolic signaling; however, NRF2 and HSR responses can also become functionally uncoupled under specific biochemical and metabolic conditions. This review critically examines the molecular mechanisms underlying NRF2-HSP crosstalk and its functional consequences in neurodegeneration, cancer, ischemia-reperfusion (I/R) injury, aging, and tumor immunity. Particular attention is given to the dual role of this axis: transient activation promotes cytoprotection, proteostasis, and tissue recovery, whereas chronic or constitutive activation can support tumor metabolism, immune evasion, and therapeutic resistance. In I/R injury, endoplasmic reticulum (ER) stress (ERS)-induced XBP1-HRD1 signaling may impose an additional constraint on NRF2 activity, highlighting an important limitation of endogenous cytoprotection. Finally, we discuss therapeutic strategies targeting NRF2, HSF1, and HSPs, emphasizing the challenges of systemic pathway modulation, the importance of pharmacodynamic biomarkers and molecular stratification, and the potential of rational combination approaches. A context-, tissue-, and cell-specific understanding of NRF2-HSP signaling will be essential for translating this complex stress-response network into precision therapeutic strategies.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e8809922"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655766/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149170255","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}
引用次数: 0
RETRACTION: Protocatechuic Acid Prevents oxLDL-Induced Apoptosis by Activating JNK/Nrf2 Survival Signals in Macrophages. 原儿茶酸通过激活巨噬细胞的JNK/Nrf2存活信号来阻止氧化ldl诱导的细胞凋亡。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-01 DOI: 10.1155/omcl/9898245
Oxidative Medicine And Cellular Longevity
{"title":"RETRACTION: Protocatechuic Acid Prevents oxLDL-Induced Apoptosis by Activating JNK/Nrf2 Survival Signals in Macrophages.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9898245","DOIUrl":"10.1155/omcl/9898245","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9898245"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13056694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147634000","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}
引用次数: 0
RETRACTION: Chitoheptaose Promotes Heart Rehabilitation in a Rat Myocarditis Model by Improving Antioxidant, Anti-Inflammatory, and Antiapoptotic Properties. 撤回:壳七糖通过改善抗氧化、抗炎和抗凋亡特性促进大鼠心肌炎模型的心脏康复。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-01 DOI: 10.1155/omcl/9864523
Oxidative Medicine And Cellular Longevity
{"title":"RETRACTION: Chitoheptaose Promotes Heart Rehabilitation in a Rat Myocarditis Model by Improving Antioxidant, Anti-Inflammatory, and Antiapoptotic Properties.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9864523","DOIUrl":"10.1155/omcl/9864523","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9864523"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140287/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147581992","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}
引用次数: 0
RETRACTION: Plasma Small Extracellular Vesicle-Carried miRNA-501-5p Promotes Vascular Smooth Muscle Cell Phenotypic Modulation-Mediated In-Stent Restenosis. 收缩:血浆细胞外小泡携带的miRNA-501-5p促进血管平滑肌细胞表型调节介导的支架内再狭窄。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-01 DOI: 10.1155/omcl/9806752
Oxidative Medicine And Cellular Longevity
{"title":"RETRACTION: Plasma Small Extracellular Vesicle-Carried miRNA-501-5p Promotes Vascular Smooth Muscle Cell Phenotypic Modulation-Mediated In-Stent Restenosis.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9806752","DOIUrl":"10.1155/omcl/9806752","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9806752"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13288251/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148302665","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}
引用次数: 0
RETRACTION: Acetaldehyde Induces Neurotoxicity In Vitro via Oxidative Stress- and Ca2+ Imbalance-Mediated Endoplasmic Reticulum Stress. 缩回:乙醛通过氧化应激和Ca2+失衡介导的内质网应激诱导体外神经毒性。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-01 DOI: 10.1155/omcl/9787694
Oxidative Medicine And Cellular Longevity
{"title":"RETRACTION: Acetaldehyde Induces Neurotoxicity In Vitro via Oxidative Stress- and Ca<sup>2+</sup> Imbalance-Mediated Endoplasmic Reticulum Stress.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9787694","DOIUrl":"10.1155/omcl/9787694","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9787694"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13320807/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148361851","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}
引用次数: 0
Neuroprotective Effects of Two N-Benzylamides in Models of Oxidative Stress, Neurite Outgrowth and Neurodegeneration. 两种n -苄胺在氧化应激、神经突生长和神经退行性变模型中的神经保护作用。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-01 DOI: 10.1155/omcl/3092494
Subaraja Mamangam, Anantha Krishnan Dhanabalan, Kanika Verma, Mani Iyer Prasanth, Sirikalaya Brimson, James Michael Brimson
{"title":"Neuroprotective Effects of Two N-Benzylamides in Models of Oxidative Stress, Neurite Outgrowth and Neurodegeneration.","authors":"Subaraja Mamangam, Anantha Krishnan Dhanabalan, Kanika Verma, Mani Iyer Prasanth, Sirikalaya Brimson, James Michael Brimson","doi":"10.1155/omcl/3092494","DOIUrl":"10.1155/omcl/3092494","url":null,"abstract":"<p><p>Oxidative stress is a central pathological mechanism in neurodegenerative diseases (NDDs), contributing to mitochondrial dysfunction, impaired proteostasis, and progressive neuronal loss. The sigma-1 receptor (S1R) is an endoplasmic reticulum (ER)-resident chaperone that coordinates cellular stress responses and has emerged as a promising therapeutic target for neuroprotection. In this study, we investigated the neuroprotective properties and mechanisms of the structurally related N-benzylamides, N-benzylcinnamide (NBCA) and N-benzylbenzamide (NBBA) using complementary in vitro, in vivo and in silico approaches. Neuroprotective activity was initially evaluated using glutamate-induced oxidative injury in HT22 hippocampal neurones and H<sub>2</sub>O<sub>2</sub>-induced oxidative stress in SH-SY5Y neuroblastoma cells. Both compounds significantly attenuated oxidative injury, although NBCA consistently showed greater efficacy and was therefore selected for detailed mechanistic investigation. NBCA reduced intracellular reactive oxygen species (ROS) production and lipid peroxidation while restoring endogenous antioxidant enzyme activities, mitochondrial membrane potential, ATP production, and cholinergic homeostasis. Immunofluorescence analysis showed that NBCA modulated nuclear factor erythroid 2-related factor 2 (NRF2) and S1R immunoreactivity after oxidative stress. NBCA also promoted neurite outgrowth in wild-type (WT) Neuro-2a cells, whereas these effects were absent in S1R knockout cells, supporting the involvement of S1R-associated signalling. Molecular docking predicted favourable interactions between NBCA and the stress-response proteins S1R, BiP and TMEM97, suggesting modulation of interconnected cellular stress-response networks. In Caenorhabditis elegans, NBCA improved resistance to oxidative stress, preserved learning and memory, delayed amyloid-β-induced paralysis, and reduced amyloid deposition in transgenic Alzheimer's disease (AD) models. Collectively, these findings demonstrate that NBCA exerts neuroprotective effects across multiple experimental models by preserving redox homeostasis, mitochondrial function, and neuronal integrity. The convergence of pharmacological, genetic, imaging, computational, and whole-organism evidence supports the involvement of S1R-associated signalling in NBCA's biological activity. Together, these findings demonstrate that modulation of S1R-associated cellular stress-response networks is a promising strategy for preserving neuronal function during oxidative stress and neurodegeneration and identify NBCA as a valuable lead compound for future mechanistic and therapeutic investigation.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e3092494"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13583929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990955","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}
引用次数: 0
RETRACTION: Capsaicin Protects Cardiomyocytes against Anoxia/Reoxygenation Injury via Preventing Mitochondrial Dysfunction Mediated by SIRT1. 撤回:辣椒素通过防止SIRT1介导的线粒体功能障碍保护心肌细胞免受缺氧/再氧化损伤。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-01 DOI: 10.1155/omcl/9813621
Oxidative Medicine And Cellular Longevity
{"title":"RETRACTION: Capsaicin Protects Cardiomyocytes against Anoxia/Reoxygenation Injury via Preventing Mitochondrial Dysfunction Mediated by SIRT1.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9813621","DOIUrl":"10.1155/omcl/9813621","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9813621"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13239129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148150744","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}
引用次数: 0
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