Redox Report最新文献_第8页

FOXO1-NMNAT3 axis dysregulation promotes doxorubicin cardiotoxicity: NAD⁺ replenishment as a redox-targeted antioxidant therapy. fox01 - nmnat3轴失调促进阿霉素心脏毒性：NAD+补充作为氧化还原靶向抗氧化治疗。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-09-29 DOI: 10.1080/13510002.2025.2565033

Fang Cheng, Minzhu Zhao, Qi Wang, Hongli Xiong, Kai Yu, Chong Chen, Ying Zhu, Yemiao Chen, Jianbo Li

{"title":"FOXO1-NMNAT3 axis dysregulation promotes doxorubicin cardiotoxicity: NAD+ replenishment as a redox-targeted antioxidant therapy.","authors":"Fang Cheng, Minzhu Zhao, Qi Wang, Hongli Xiong, Kai Yu, Chong Chen, Ying Zhu, Yemiao Chen, Jianbo Li","doi":"10.1080/13510002.2025.2565033","DOIUrl":"10.1080/13510002.2025.2565033","url":null,"abstract":"Objectives: Doxorubicin (DOX) induces dose-dependent cardiotoxicity, primarily through oxidative stress and metabolic dysregulation. Although NAD+ deficiency has been implicated in cardiovascular pathology, its role in DOX-induced cardiotoxicity (DIC) remains poorly understood. This study investigated NAD+ metabolism dysregulation as a redox-sensitive mechanism in DIC pathogenesis.Methods: Human cardiomyocytes (AC16), mouse atrial myocytes (HL-1), and C57BL/6 mice were used to establish the DIC model. The role and mechanism of NAD+ in DIC were investigated using a range of methods.Results: Using integrated in vitro and in vivo models, we demonstrated that DOX induces myocardial oxidative damage accompanied by NAD+ depletion. Exogenous NAD+ supplementation mitigated the DOX-induced cardiomyocyte death and redox imbalance. Mechanistically, pharmacological CD38 inhibition with 78C or genetic silencing failed to restore the NAD+ pool, whereas nicotinamide mononucleotide adenylyltransferase 3 (NMNAT3) overexpression, combined with nicotinamide mononucleotide (NMN) administration, effectively rescued NAD+ levels and attenuated oxidative stress. Computational and functional analyses identified FOXO1 as a transcriptional repressor of NMNAT3 following DOX exposure.Conclusion: This study establishes the dysregulation of the FOXO1-NMNAT3 axis as a key mechanism underlying NAD+ depletion in DIC. Targeting this axis through NAD+ replenishment, particularly by activating NMNAT3, offers a novel redox-based therapeutic strategy against DIC.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2565033"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12481541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145192516","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

Is uric acid a true antioxidant? Identification of uric acid oxidation products and their biological effects. 尿酸是真正的抗氧化剂吗？尿酸氧化产物的鉴定及其生物学效应。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-05-25 DOI: 10.1080/13510002.2025.2498105

Mikaela Peglow Pinz, Isadora Medeiros, Larissa Anastácio da Costa Carvalho, Flavia Carla Meotti

{"title":"Is uric acid a true antioxidant? Identification of uric acid oxidation products and their biological effects.","authors":"Mikaela Peglow Pinz, Isadora Medeiros, Larissa Anastácio da Costa Carvalho, Flavia Carla Meotti","doi":"10.1080/13510002.2025.2498105","DOIUrl":"10.1080/13510002.2025.2498105","url":null,"abstract":"Uric acid (UA), the final product of purine metabolism in humans, exhibits a dual role as an anti or pro-oxidant, depending on the microenvironment. The two-electron oxidation of UA by biological oxidants can neutralize such harmful molecules. Additionally, UA chelates metals and can activate adaptive response against oxidation. However, some products of the reaction between UA and oxidants are not inert and, therefore, do not confer the anticipated antioxidant protection. A direct pro-oxidant effect is favoured in the one-electron oxidation of UA by heme-peroxidases yielding free radical intermediates that can initiate or propagate a radical-chain reaction. Additionally, an indirect pro-oxidant effect has been proposed by eliciting the expression or activation of enzymes that catalyse oxidant production, e.g. NADPH oxidase (NOX). This review brings together fundamental concepts and the molecular mechanisms of the redox reactions involving UA. The signature metabolites from these reactions are discussed to give valuable insights on whether these intermediates are being formed and what role they may play in disease pathogenesis. It proposes that, through identifying specific products, it may be possible to elucidate whether a harmful or protective action is linked to downstream bioactivities.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2498105"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12107670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143405","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

Zinc nanoparticles mitigate azoxystrobin and its nanoencapsulation-induced hepatic and renal toxicity in rats. 锌纳米颗粒减轻氮嘧菌酯及其纳米包封引起的大鼠肝、肾毒性。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-04-20 DOI: 10.1080/13510002.2025.2491318

Nashwa Elshaer, Ahmed M Eldeeb, Ahmed A A Aioub, Ahmed S Hashem, Soumya Ghosh, Lamya Ahmed Alkeridis, Mohammed Ali Alshehri, Mustafa Shukry, Daklallah A Almalki, Hind A Alkhatabi, Mohamed Afifi, Ammar Al-Farga, Mohamed A Hendawy, Ahmed E A El-Sobki

{"title":"Zinc nanoparticles mitigate azoxystrobin and its nanoencapsulation-induced hepatic and renal toxicity in rats.","authors":"Nashwa Elshaer, Ahmed M Eldeeb, Ahmed A A Aioub, Ahmed S Hashem, Soumya Ghosh, Lamya Ahmed Alkeridis, Mohammed Ali Alshehri, Mustafa Shukry, Daklallah A Almalki, Hind A Alkhatabi, Mohamed Afifi, Ammar Al-Farga, Mohamed A Hendawy, Ahmed E A El-Sobki","doi":"10.1080/13510002.2025.2491318","DOIUrl":"https://doi.org/10.1080/13510002.2025.2491318","url":null,"abstract":"This study sought to ascertain if zinc nanoparticles (ZnNPs) could lessen the toxicity of azoxystrobin (AZ). This naturally occurring methoxyacrylate is one of the most often used fungicides in agriculture in male albino rats. Six sets of 60 mature male albino rats were randomly assigned: control (distilled water), Azoxystrobin formulation (AZOF), Azoxystrobin nano-formula (AZON), ZnNPs, AZOF + ZnNPs, and AZON + ZnNPs. Blood and tissues were obtained for further immunohistochemical, pathological, and biochemical examination. The results showed that exposure to AZOF and AZON significantly increased the levels of the oxidative stress indicators glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA). Additionally, AZOF significantly impacts liver function bioindicators, including aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. AZOF and AZON induced damage to the liver and kidney by disrupting vascular dilatation and causing hemorrhages, apoptosis, inflammatory lymphocytes, and necrosis. Furthermore, co-administration of ZnNPs with fungicides (AZOF and AZON) can gently enhance the alterations of oxidative stress and liver function bioindicators levels. These findings showed that ZnNPs could help male rats receiving AZ treat their histologically abnormal liver and kidney.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2491318"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12010655/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143996445","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

The novel thioredoxin reductase inhibitor butaselen suppresses lung cancer by inducing oxidative stress. 新型硫氧还蛋白还原酶抑制剂丁塞伦通过诱导氧化应激抑制肺癌。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-11-26 DOI: 10.1080/13510002.2025.2588086

Yifan Chen, Guangliang Qiang, Liang Jin, Yan Sun, Guozhou Zhang, Fengling Hu, Jinhui Feng, Feng Wei, Shengxin Zeng, Lixiang Xue, Huihui Zeng, Shaohua Ma

{"title":"The novel thioredoxin reductase inhibitor butaselen suppresses lung cancer by inducing oxidative stress.","authors":"Yifan Chen, Guangliang Qiang, Liang Jin, Yan Sun, Guozhou Zhang, Fengling Hu, Jinhui Feng, Feng Wei, Shengxin Zeng, Lixiang Xue, Huihui Zeng, Shaohua Ma","doi":"10.1080/13510002.2025.2588086","DOIUrl":"10.1080/13510002.2025.2588086","url":null,"abstract":"Background: Lung cancer is one of the leading causes of cancer-related deaths worldwide with limited treatment options available. The anti-tumor effects of the TrxR inhibitor Butaselen (BS/BS1801) on lung cancer and its underlying mechanisms remain unknown.Methods: This study utilized lung cancer cell lines, LLC1-bearing mice models, and organoids to detect the inhibitory effects of BS on lung cancer. The ROS-induction and apoptotic role of BS on lung cancer cells and molecular mechanisms were assessed with flow cytometry, western blot, Co-IP, real-time PCR, ChIP, reporter gene assay, ELISA, and bisulfite pyrosequencing.Results: BS can effectively inhibit lung cancer both in vitro and in vivo, by triggering ROS-induced apoptosis. The inactivation of NF-κB and MAPK signaling pathways, along with the activation of PI3K-Akt and HBP1 signaling pathways, are involved in BS's suppression of lung cancer. HBP1 is a novel downstream target of the Trx system. The activation of HBP1 by BS is dependent on ROS accumulation and further leads to the transcriptional inhibition of DNMT1 and the demethylation of the whole genome, as well as the promoters of p21 and HOXA9.Conclusion: The TrxR/Trx inhibitor butaselen suppresses lung cancer by triggering ROS-induced apoptosis. This study provides a novel and effective regimen for treating lung cancer.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2588086"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12667355/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145605592","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

Statement of Retraction: Prophylactic role of Enhydra fluctuans against arsenic-induced hepatotoxicity via antiapoptotic and antioxidant mechanisms. 撤回声明：Enhydra波动通过抗凋亡和抗氧化机制预防砷诱导的肝毒性。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-08-04 DOI: 10.1080/13510002.2025.2538364

引用次数: 0

YY1-induced Long non-coding RNA HOXA11-AS activates oxidative stress and inflammation by epigenetic modification of Nrf2 pathway to promote keloid formation. yy1诱导的长链非编码RNA HOXA11-AS通过表观遗传修饰Nrf2通路激活氧化应激和炎症，促进瘢痕疙瘩形成。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-08-12 DOI: 10.1080/13510002.2025.2539030

Jun Jin, Kai Wang, Chenxi Lu, Chenghao Yao, Feng Xie

{"title":"YY1-induced Long non-coding RNA HOXA11-AS activates oxidative stress and inflammation by epigenetic modification of Nrf2 pathway to promote keloid formation.","authors":"Jun Jin, Kai Wang, Chenxi Lu, Chenghao Yao, Feng Xie","doi":"10.1080/13510002.2025.2539030","DOIUrl":"10.1080/13510002.2025.2539030","url":null,"abstract":"Background: Long non-coding RNAs (lncRNAs) are increasingly recognized in keloid pathogenesis. This study investigates the role and mechanisms of HOXA11-AS in keloid formation.Methods: Expression levels of HOXA11-AS and related proteins were measured in keloid tissues and fibroblasts using qRT-PCR, Western blot, and ELISA. Functional assays assessed cell proliferation, migration, fibrosis, and oxidative stress. RIP, ChIP, Co-IP, FISH, and luciferase assays were used to explore interactions among HOXA11-AS, YY1, Nrf2, EZH2, and DNMT1. An in vivo mouse xenograft model validated the findings.Results: HOXA11-AS was upregulated in keloids. Silencing HOXA11-AS reduced fibroblast proliferation, migration, fibrosis, and oxidative stress. Its overexpression had the opposite effect, which was reversed by Nrf2 pathway inhibition. HOXA11-AS promoted the methylation of the Nrf2 promoter via DNMT1 recruitment, mediated by EZH2. YY1 enhanced HOXA11-AS transcription by binding to its promoter. The YY1/HOXA11-AS axis was confirmed in vivo.Conclusion: YY1-induced HOXA11-AS drives keloid formation by promoting oxidative stress and inflammation through epigenetic suppression of Nrf2 signaling.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2539030"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144837449","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

Cystathionine γ-lyase downregulation promotes liver injury and necroptosis through reprogramming of methionine cycle. 半胱硫氨酸γ-裂解酶下调通过蛋氨酸循环重编程促进肝损伤和坏死下垂。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-07-28 DOI: 10.1080/13510002.2025.2531650

Cichun Wu, Wei Zhang, Wenhu Liu, Zhengshan Tang, Shifang Peng, Lei Fu, Xin Ni

{"title":"Cystathionine γ-lyase downregulation promotes liver injury and necroptosis through reprogramming of methionine cycle.","authors":"Cichun Wu, Wei Zhang, Wenhu Liu, Zhengshan Tang, Shifang Peng, Lei Fu, Xin Ni","doi":"10.1080/13510002.2025.2531650","DOIUrl":"10.1080/13510002.2025.2531650","url":null,"abstract":"Objective: Chronic liver diseases (CLDs) are prevalent globally. The purpose of the current study was to elucidate the regulatory mechanisms underlying the pathophysiological processes in CLDs.Methods and results: Using the GEO database, we identified cysteine and methionine metabolism as a commonly enriched pathway in some CLDs. We then confirmed that hepatic cystathionine γ-lyase (Cth), a key enzyme in this pathway, was significantly downregulated in some CLDs in humans and rodent models. Cth-deficient mice exhibited hepatic necroptosis, inflammation and mitochondrial impairment. Omics revealed methionine cycle dysregulation and reduced betaine, a methionine cycle metabolite. Betaine supplementation rewired the methionine cycle, and alleviated necroptosis, inflammation and mitochondrial impairment. Dysregulation of fatty acid β-oxidation, glycolysis and lipid biosynthesis caused by Cth deficiency was improved by betaine. Cth deficiency decreased Pparα, Nrf2, Pgc-1α, and Srebf2 (the transcription factors linked to mitochondria function and metabolism) expression while increasing Irf8 and Irf9, changes reversed by betaine. Histone methylation (H3K9me3, H3K27me3, H3K79me3) decreased, and acetylation (H3K27ac) increased with Cth deficiency, which betaine corrected. Irf8 and Irf9 and Ppara and Ppargc1a expression were regulated by H3K27me3 and H3K79me3 in hepatocytes, respectively.Discussion: Our study indicates that CTH is the key factor for maintaining hepatocyte function and survival through homeostasis of the methionine cycle and immediately highlights a new potential target of hepatic protection therapy for some CLDs.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2531650"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12305881/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144733002","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

Redox-dependent activation of protein kinase G1α contributes to transient receptor potential cation channel subfamily V member 1-mediated acute nociceptive pain behavior. 蛋白激酶G1α的氧化还原依赖性激活有助于瞬时受体电位阳离子通道亚家族V成员1介导的急性伤害性疼痛行为。

IF 7.4 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-08-25 DOI: 10.1080/13510002.2025.2549954

Tim Berg, Katharina Metzner, Nabil Bahrami, Elena Wang, Maximilian Koch, Philip Eaton, Achim Schmidtko, Wiebke Kallenborn-Gerhardt

{"title":"Redox-dependent activation of protein kinase G1α contributes to transient receptor potential cation channel subfamily V member 1-mediated acute nociceptive pain behavior.","authors":"Tim Berg, Katharina Metzner, Nabil Bahrami, Elena Wang, Maximilian Koch, Philip Eaton, Achim Schmidtko, Wiebke Kallenborn-Gerhardt","doi":"10.1080/13510002.2025.2549954","DOIUrl":"https://doi.org/10.1080/13510002.2025.2549954","url":null,"abstract":"Background: Sensory neurons relay the pain signals to the brain via the nociceptive system. Notably, reactive oxygen species (ROS) serve as signaling molecules in the somatosensory system; however, their contribution to sensing noxious stimuli remains poorly understood.Methods: Herein, the role of protein kinase G (PKG)1α, which is highly expressed in sensory neurons and serves as a ROS target, was investigated in sensory neurons in the processing of acute nociceptive pain. Cys42Ser PKG1α-knock-in (PKG1α-KI) mice, devoid of redox-dependent PKG1α activation, were subjected to behavioral testing, ROS detection assays, gene expression experiments, and imaging analyses.Results: Interestingly, PKG1α-KI mice showed reduced behavioral responses to noxious heat and the transient receptor potential cation channel subfamily V member 1 (TRPV1) agonist capsaicin. Moreover, capsaicin-induced sensory neuron stimulation upregulated ROS production and redox-dependent PKG1α activation. Calcium imaging results and patch-clamp recordings revealed that capsaicin-induced calcium flux and neuronal excitability was reduced in sensory neurons of PKG1α-KI mice.Conclusion: Altogether, the findings of this study show the effects of redox-dependent PKG1α activation on capsaicin/TRPV1-mediated signaling in sensory neurons during acute nociceptive pain.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"1-17"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12379704/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144966824","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

Fucoxanthin alleviates renal aging by regulating the oxidative stress process and the inflammatory response in vitro and in vivo models. 岩藻黄素通过调节体内和体外模型的氧化应激过程和炎症反应来缓解肾脏衰老。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-06-09 DOI: 10.1080/13510002.2025.2511458

Xiaomei Zhang, Weidong Qiang, Yongxin Guo, Jingli Gong, Huan Yu, Di Wu, Pengxiang Tang, Ma Yidan, Huifeng Zhang, Xin Sun

{"title":"Fucoxanthin alleviates renal aging by regulating the oxidative stress process and the inflammatory response in vitro and in vivo models.","authors":"Xiaomei Zhang, Weidong Qiang, Yongxin Guo, Jingli Gong, Huan Yu, Di Wu, Pengxiang Tang, Ma Yidan, Huifeng Zhang, Xin Sun","doi":"10.1080/13510002.2025.2511458","DOIUrl":"10.1080/13510002.2025.2511458","url":null,"abstract":"Objectives: Many countries in the world are entering society with an aging population. The kidney is one of the most sensitive organs in the body to aging. Kidney function gradually declines with aging. Renal aging is one of the main triggers of CDK. Therefore, many researchers in the field are looking for natural, green and healthy anti-renal-aging bioactive molecules.Methods and results: Western-blot, ELISA and indirect immunofluorescence were performed to evaluate the biological activity of fucoxanthin against renal aging in vitro and in vivo models. First, in the in vitro model, we evaluated the effect of fucoxanthin on renal cell senescence. We found that fucoxanthin could alleviate the kidney cell senescence caused by H2O2 by detecting a series of senescence markers. In the in vivo model, the experimental results showed that fucoxanthin could alleviate the aging of the kidney by Sa-β-gal staining and detection of aging-related marker molecules. Furthermore, we also found that fucoxanthin could alleviate kidney fibrosis.Conclusions: In this study, our results showed that fucoxanthin was able to alleviate renal aging in vivo and in vitro models, suggesting that fucoxanthin could be a functional food to treat and relieve kidney aging.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2511458"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12150648/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144258910","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

Update on the correlation between mitochondrial function and osteonecrosis of the femoral head osteocytes. 线粒体功能与股骨头骨细胞骨坏死相关性的研究进展。

IF 6.9 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-04-18 DOI: 10.1080/13510002.2025.2491846

Chengming Li, Hangyu Ji, Suyang Zhuang, Xinhui Xie, Daping Cui, Cong Zhang

{"title":"Update on the correlation between mitochondrial function and osteonecrosis of the femoral head osteocytes.","authors":"Chengming Li, Hangyu Ji, Suyang Zhuang, Xinhui Xie, Daping Cui, Cong Zhang","doi":"10.1080/13510002.2025.2491846","DOIUrl":"10.1080/13510002.2025.2491846","url":null,"abstract":"Mitochondrial health is maintained in a steady state through mitochondrial dynamics and autophagy processes. Recent studies have identified healthy mitochondria as crucial regulators of cellular function and survival. This process involves adenosine triphosphate (ATP) synthesis by mitochondrial oxidative phosphorylation (OXPHOS), regulation of calcium metabolism and inflammatory responses, and intracellular oxidative stress management. In the skeletal system, they participate in the regulation of cellular behaviors and the responses of osteoblasts, osteoclasts, chondrocytes, and osteocytes to external stimuli. Indeed, mitochondrial damage or dysfunction occurs in the development of a few bone diseases. For example, mitochondrial damage may lead to an imbalance in osteoblasts and osteoclasts, resulting in osteoporosis, osteomalacia, or poor bone production, and chondrocyte death and inflammatory infiltration in osteoarthritis are the main causes of cartilage degeneration due to mitochondrial damage. However, the opposite exists for osteosarcoma, where overactive mitochondrial metabolism is able to accelerate the proliferation and migration of osteosarcoma cells, which is a major disease feature. Bone is a dynamic organ and osteocytes play a fundamental role in all regions of bone tissue and are involved in regulating bone integrity. This review examines the impact of mitochondrial physiological function on osteocyte health and summarizes the microscopic molecular mechanisms underlying its effects. It highlights that targeted therapies focusing on osteocyte mitochondria may be beneficial for osteocyte survival, providing a new insight for the diagnosis, prevention, and treatment of diseases associated with osteocyte death.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2491846"},"PeriodicalIF":6.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12010656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144042067","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