Redox Report最新文献

MSC-mediated mitochondrial transfer promotes metabolic reprograming in endothelial cells and vascular regeneration in ARDS. 间质干细胞介导的线粒体转移促进ARDS内皮细胞的代谢重编程和血管再生。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-03-13 DOI: 10.1080/13510002.2025.2474897

Jinlong Wang, Shanshan Meng, Yixuan Chen, Haofei Wang, Wenhan Hu, Shuai Liu, Lili Huang, Jingyuan Xu, Qing Li, Xiaojing Wu, Wei Huang, Yingzi Huang

{"title":"MSC-mediated mitochondrial transfer promotes metabolic reprograming in endothelial cells and vascular regeneration in ARDS.","authors":"Jinlong Wang, Shanshan Meng, Yixuan Chen, Haofei Wang, Wenhan Hu, Shuai Liu, Lili Huang, Jingyuan Xu, Qing Li, Xiaojing Wu, Wei Huang, Yingzi Huang","doi":"10.1080/13510002.2025.2474897","DOIUrl":"10.1080/13510002.2025.2474897","url":null,"abstract":"Background: Mesenchymal stem cells (MSCs) are a potential therapy for acute respiratory distress syndrome (ARDS), but their mechanisms in repairing mitochondrial damage in ARDS endothelial cells remain unclear.Methods: We first examined MSCs' mitochondrial transfer ability and mechanisms to mouse pulmonary microvascular endothelial cells (MPMECs) in ARDS. Then, we investigated how MSC-mediated mitochondrial transfer affects the repair of endothelial damage. Finally, we elucidated the mechanisms by which MSC-mediated mitochondrial transfer promotes vascular regeneration.Results: Compared to mitochondrial-damaged MSCs, normal MSCs showed a significantly higher mitochondrial transfer rate to MPMECs, with increases of 41.68% in vitro (P < 0.0001) and 10.50% in vivo (P = 0.0005). Furthermore, MSC-mediated mitochondrial transfer significantly reduced reactive oxygen species (P < 0.05) and promoted proliferation (P < 0.0001) in MPMECs. Finally, MSC-mediated mitochondrial transfer significantly increased the activity of the tricarboxylic acid (TCA) cycle (MD of CS mRNA: 23.76, P = 0.032), and further enhanced fatty acid synthesis (MD of FAS mRNA: 6.67, P = 0.0001), leading to a 6.7-fold increase in vascular endothelial growth factor release from MPMECs and promoted vascular regeneration in ARDS.Conclusion: MSC-mediated mitochondrial transfer to MPMECs activates the TCA cycle and fatty acid synthesis, promoting endothelial proliferation and pro-angiogenic factor release, thereby enhancing vascular regeneration in ARDS.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2474897"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11912292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625694","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

Rotenone inhibited osteosarcoma metastasis by modulating ZO-2 expression and location via the ROS/Ca²⁺/AMPK pathway. 鱼藤酮通过ROS/Ca2+/AMPK通路调节ZO-2的表达和定位，从而抑制骨肉瘤转移。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-04-17 DOI: 10.1080/13510002.2025.2493556

Xiang Ma, Zhen Li, Hengwei Ma, Kun Jiang, Bao Chen, Weiquan Wang, Ziqiang Zhu, Jianqiang Wang, Zuozhang Yang, Wang Yunqing, Suwei Dong

{"title":"Rotenone inhibited osteosarcoma metastasis by modulating ZO-2 expression and location via the ROS/Ca2+/AMPK pathway.","authors":"Xiang Ma, Zhen Li, Hengwei Ma, Kun Jiang, Bao Chen, Weiquan Wang, Ziqiang Zhu, Jianqiang Wang, Zuozhang Yang, Wang Yunqing, Suwei Dong","doi":"10.1080/13510002.2025.2493556","DOIUrl":"https://doi.org/10.1080/13510002.2025.2493556","url":null,"abstract":"Background: Pulmonary metastases in osteosarcoma (OS) are associated with a poor prognosis. Rotenone has shown anti-cancer activity. However, its effects on metastasis and the underlying mechanisms remain unknown. This study investigated the potential use of Rotenone for OS treatment.Methods: The effect of Rotenone and ROS/Ca2+/AMPK/ZO-2 pathway on metastasis and EMT was evaluated by Western blot, Transwell and Wound healing. Flow cytometer was employed to measure the intracellular Ros and Ca2+ levels. The subcellular location of ZO-2 was detected by IF, interaction between AMPK and ZO-2 were examined by Co-IP. Then, subcutaneous tumor and metastasis models were used to evaluate the function of Rotenone in OS metastasis.Results: Rotenone-induced ROS led to increased intracellular Ca2+, which promoted the EMT of OS cells through activation of AMPK and ZO-2 nuclear translocation. Inhibition of ROS production decreased intracellular Ca2+, restraining AMPK activity. Knock-down of ZO-2 significantly suppressed the anti-metastasis effects of Rotenone in OS cells. Moreover, Rotenone elevated p-AMPK and ZO-2 expression but inhibited EMT and lung metastasis in vivo.Conclusion These results provide evidence supporting an anti-metastatic effect of Rotenone. These findings support the use of Rotenone in the prevention of OS metastasis.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2493556"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12010658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144010184","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

Varespladib attenuates Naja atra-induced acute liver injury via reversing Nrf2 signaling-mediated ferroptosis and mitochondrial dysfunction. Varespladib通过逆转Nrf2信号介导的铁下垂和线粒体功能障碍，减轻Naja atra诱导的急性肝损伤。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-05-21 DOI: 10.1080/13510002.2025.2507557

Jiahao Liu, Linfeng Wang, Mengxia Xie, Wenjie Zhao, Jiaqi Sun, Yuji Jin, Meiling Liu, Jianqi Zhao, Lixia Cheng, Cheng Wen, Xiaowen Bi, Chunhong Huang

{"title":"Varespladib attenuates Naja atra-induced acute liver injury via reversing Nrf2 signaling-mediated ferroptosis and mitochondrial dysfunction.","authors":"Jiahao Liu, Linfeng Wang, Mengxia Xie, Wenjie Zhao, Jiaqi Sun, Yuji Jin, Meiling Liu, Jianqi Zhao, Lixia Cheng, Cheng Wen, Xiaowen Bi, Chunhong Huang","doi":"10.1080/13510002.2025.2507557","DOIUrl":"10.1080/13510002.2025.2507557","url":null,"abstract":"Objective: To investigate the protective effects of varespladib against Naja atra-induced acute liver injury (ALI) and to elucidate the toxic mechanism of snake venom phospholipase A2 (SVPLA2)-induced hepatic oxidative stress, with a particular focus on the role of Nrf2 signaling and its downstream pathways.Methods: A combination of in vivo and in vitro models of N. atra envenomation was employed to assess liver injury, oxidative stress, and mitochondrial dysfunction. The interaction between SVPLA2 and Nrf2 was analyzed, and the effects of varespladib treatment on these processes were evaluated using histological analysis, biochemical assays, and molecular techniques targeting oxidative stress, ferroptosis, mitophagy, and apoptosis.Results: Varespladib significantly alleviated N. atra-induced ALI. SVPLA2 was found to directly bind to Nrf2, leading to severe oxidative stress. This oxidative stress initiated a cascade involving Nrf2-mediated ferroptosis, mitochondrial dysfunction, excessive mitophagy, and mitochondria-dependent apoptosis. Treatment with varespladib effectively reversed these pathological events by inhibiting SVPLA2 activity.Conclusion: Varespladib shows strong therapeutic potential for N. atra envenomation by targeting SVPLA2. Nrf2 was identified as a direct toxic target of SVPLA2, and Nrf2-mediated ferroptosis and mitochondrial dysfunction were key mechanisms underlying SVPLA2-induced hepatic injury.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2507557"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12096701/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144120477","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

METTL14 Mediates Glut3 m6A methylation to improve osteogenesis under oxidative stress condition. METTL14介导Glut3 m6A甲基化促进氧化应激条件下的成骨。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2024-12-31 DOI: 10.1080/13510002.2024.2435241

Ying Wang, Xueying Yu, Fenyong Sun, Yan Fu, Tingting Hu, Qiqing Shi, Qiuhong Man

{"title":"METTL14 Mediates Glut3 m6A methylation to improve osteogenesis under oxidative stress condition.","authors":"Ying Wang, Xueying Yu, Fenyong Sun, Yan Fu, Tingting Hu, Qiqing Shi, Qiuhong Man","doi":"10.1080/13510002.2024.2435241","DOIUrl":"https://doi.org/10.1080/13510002.2024.2435241","url":null,"abstract":"Objectives: Bone remodeling imbalance contributes to osteoporosis. Though current medications enhance osteoblast involvement in bone formation, the underlying pathways remain unclear. This study was aimed to explore the pathways involved in bone formation by osteoblasts, we investigate the protective role of glycolysis and N6-methyladenosine methylation (m6A) against oxidative stress-induced impairment of osteogenesis in MC3T3-E1 cells.Methods: We utilized a concentration of 200 μM hydrogen peroxide (H2O2) to establish an oxidative damage model of MC3T3-E1 cells. Subsequently, we examined the alterations in the m6A methyltransferases (METTL3, METTL14), glucose transporter proteins (GLUT1, GLUT3) and validated m6A methyltransferase overexpression in vitro and in an osteoporosis model. The osteoblast differentiation and osteogenesis-related molecules and serum bone resorption markers were measured by biochemical analysis, Alizarin Red S staining, Western blot and ELISA.Results: H2O2 treatment inhibited glycolysis and osteoblast differentiation in MC3T3-E1 cells. However, when METTL14 was overexpressed, these changes induced by H2O2 could be mitigated. Our findings indicate that METTL14 promotes GLUT3 expression via YTHDF1, leading to the modulation of various parameters in the H2O2-induced model. Similar positive effects of METTL14 on osteogenesis were observed in an ovariectomized mouse osteoporosis model.Discussion: METTL14 could serve as a potential therapeutic approach for enhancing osteoporosis treatment.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2435241"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142906897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Remimazolam induced cytotoxicity mediated through multiple stress pathways and acted synergistically with tyrosine kinase inhibitors in hepatocellular carcinoma. 雷马唑仑通过多种应激途径诱导细胞毒性，并与酪氨酸激酶抑制剂协同作用于肝细胞癌。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-03-07 DOI: 10.1080/13510002.2025.2475696

Hsiu-Lung Fan, Jia-Lin Chen, Shu-Ting Liu, Jia-Tong Lee, Shih-Ming Huang, Zhi-Fu Wu, Hou-Chuan Lai

{"title":"Remimazolam induced cytotoxicity mediated through multiple stress pathways and acted synergistically with tyrosine kinase inhibitors in hepatocellular carcinoma.","authors":"Hsiu-Lung Fan, Jia-Lin Chen, Shu-Ting Liu, Jia-Tong Lee, Shih-Ming Huang, Zhi-Fu Wu, Hou-Chuan Lai","doi":"10.1080/13510002.2025.2475696","DOIUrl":"10.1080/13510002.2025.2475696","url":null,"abstract":"The primary treatment for hepatocellular carcinoma (HCC) involves surgical removal of the primary tumor, but this creates a favorable environment for the proliferation and spread of residual and circulating cancer cells. The development of remimazolam-based balanced anesthesia is crucial for future antitumor applications. It is important to understand the mechanisms of cytotoxicity for HCC in detail.We performed cell viability analysis, western blotting analysis, reverse transcription-polymerase chain reaction analysis, and flow cytometry analysis in two HCC cell lines, HepG2 and Hep3B cells.Our data demonstrated that remimazolam induced cytotoxicity by suppressing cell proliferation, inhibiting G1 phase progression, and affecting mitochondrial reactive oxygen species (ROS) levels, leading to apoptosis, DNA damage, cytosolic ROS elevation, lipid peroxidation, autophagy, mitochondrial depolarization, and endoplasmic reticulum stress. Inhibitors of apoptosis, autophagic cell death, and ferroptosis and a ROS scavenger failed to rescue cell death caused by remimazolam besylate. Our combination index revealed that remimazolam besylate has the potential to act as a sensitizer for targeted tyrosine kinase inhibitor therapy for HCC.Our findings open up new possibilities for combinatory HCC therapy using remimazolam, leveraging its dual functional roles in surgery and drug therapy for liver cancers.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2475696"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11892054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143575824","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

Involvement of oxidative stress in post-acute sequelae of COVID-19: clinical implications. 氧化应激参与COVID-19急性后后遗症：临床意义

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-03-03 DOI: 10.1080/13510002.2025.2471738

Paola Mayara Valente Coronel, Denise Caroline Luiz Soares Basilio, Isabelly Teixeira Espinoça, Kamylla Fernanda Souza de Souza, Nathalia Miranda Campos, Rafael Seiji Nakano Ota, Edgar Julian Paredes-Gamero, Danilo Wilhelm Filho, Ana Rita Coimbra Motta-Castro, Renata Trentin Perdomo, Eduardo Benedetti Parisotto

{"title":"Involvement of oxidative stress in post-acute sequelae of COVID-19: clinical implications.","authors":"Paola Mayara Valente Coronel, Denise Caroline Luiz Soares Basilio, Isabelly Teixeira Espinoça, Kamylla Fernanda Souza de Souza, Nathalia Miranda Campos, Rafael Seiji Nakano Ota, Edgar Julian Paredes-Gamero, Danilo Wilhelm Filho, Ana Rita Coimbra Motta-Castro, Renata Trentin Perdomo, Eduardo Benedetti Parisotto","doi":"10.1080/13510002.2025.2471738","DOIUrl":"10.1080/13510002.2025.2471738","url":null,"abstract":"Oxidative stress (OS) plays a key role in the pathophysiology of COVID-19 and may be associated with sequelae after severe SARS-CoV-2 infection. This study evaluated OS and inflammation biomarkers in blood from individuals with post-acute sequelae of COVID-19 (PASC). 64 male and female participants were distributed into three groups: healthy individuals (n = 20), acute COVID-19 patients (symptoms for <3 weeks, n = 15), and PASC patients (symptoms for >12 weeks, n = 29). Analyses included inflammatory cytokines, myeloperoxidase (MPO) activity, and OS markers, such as superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), gamma-glutamyl transferase (GGT), reduced glutathione (GSH), uric acid (UA), thiobarbituric acid reactive substances (TBARS), and protein carbonyls (PC). Individuals with PASC showed increased IL-6 and IL-8. Both COVID-19 groups exhibited decreased SOD and CAT. GST decreased only in the acute group. Elevated GGT and GSH were found in the PASC group. High UA levels were observed in PASC individuals. There were no changes in TBARS values ⁣⁣in the PASC group. However, PC concentrations were elevated only in this group. Correlations were identified between inflammatory markers and OS parameters. These findings suggest that individuals with PASC pronounced OS, which potentially exacerbates disease complications. Monitoring OS biomarkers could aid in patient prognosis and management.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2471738"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143543369","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

ACSF2-PGK1 interaction promotes ferroptosis in renal tubular epithelial cells of diabetic nephropathy by regulating Keap1/Nrf2 signaling. ACSF2-PGK1相互作用通过调节Keap1/Nrf2信号通路促进糖尿病肾病肾小管上皮细胞铁下垂。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-07-16 DOI: 10.1080/13510002.2025.2529618

Xinran Liu, Chaoyi Chen, Sai Zhu, Xiaomei Luo, Li Gao, Ziyun Hu, Yu Ma, Ling Jiang, Yonggui Wu

{"title":"ACSF2-PGK1 interaction promotes ferroptosis in renal tubular epithelial cells of diabetic nephropathy by regulating Keap1/Nrf2 signaling.","authors":"Xinran Liu, Chaoyi Chen, Sai Zhu, Xiaomei Luo, Li Gao, Ziyun Hu, Yu Ma, Ling Jiang, Yonggui Wu","doi":"10.1080/13510002.2025.2529618","DOIUrl":"10.1080/13510002.2025.2529618","url":null,"abstract":"Objectives: Recent studies have highlighted the strong association between kidney disease and ferroptosis. However, the role of ferroptosis in diabetic nephropathy (DN) remains unclear. This study aimed to determine the role of ACSF2 in renal tubule injury in DN and its underlying mechanisms.Methods: We established diabetic kidney disease models both in vivo, using db/db mice, and in vitro, using high glucose induced HK-2 cells.Results: A significant upregulation of ACSF2 was observed in the renal tubules of patients with DN and db/db mice. ACSF2 expression correlated with renal tubule injury and renal function, indicating its potential as an independent biomarker in patients with DN. Silencing ACSF2 alleviated high glucose-induced renal tubular epithelial cell injury by reducing oxidative stress-induced ferroptosis in vivo and in vitro. Mechanistically, liquid chromatography-tandem mass spectrometry and co-immunoprecipitation demonstrated that ACSF2 specifically binds to PGK1. ACSF2 affected Keap1 dimerization by regulating PGK1 phosphorylation at serine 203, which subsequently affects the levels of NRF2. Moreover, PGK1 stabilizes ACSF2 via deubiquitination, establishing a positive feedback loop. The results provide evidence that the interaction between ACSF2 and PGK1 promotes DN progression by regulating oxidative stress-induced ferroptosis.Discussion: ACSF2 participates in crosstalk between oxidative stress and ferroptosis. This could be a potential therapeutic target for DN.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2529618"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144650221","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

ASIC1a Promotes nucleus pulposus derived stem cells apoptosis through modulation of SIRT3-dependent mitochondrial redox homeostasis in intervertebral disc degeneration. ASIC1a通过调节椎间盘退变中sirt3依赖的线粒体氧化还原稳态，促进髓核来源的干细胞凋亡。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2025-07-08 DOI: 10.1080/13510002.2025.2504120

Zhi-Gang Zhang, Liang Kang, Lu-Ping Zhou, Yan-Xin Wang, Chong-Yu Jia, Chen-Hao Zhao, Bo Zhang, Jia-Qi Wang, Hua-Qing Zhang, Ren-Jie Zhang, Cai-Liang Shen

{"title":"ASIC1a Promotes nucleus pulposus derived stem cells apoptosis through modulation of SIRT3-dependent mitochondrial redox homeostasis in intervertebral disc degeneration.","authors":"Zhi-Gang Zhang, Liang Kang, Lu-Ping Zhou, Yan-Xin Wang, Chong-Yu Jia, Chen-Hao Zhao, Bo Zhang, Jia-Qi Wang, Hua-Qing Zhang, Ren-Jie Zhang, Cai-Liang Shen","doi":"10.1080/13510002.2025.2504120","DOIUrl":"10.1080/13510002.2025.2504120","url":null,"abstract":"The death of human nucleus pulposus derived stem cells (NPSCs) is a key factor affecting the endogenous repair capability and degeneration of intervertebral discs (IVD). ASIC1a is thought to be closely associated with cells destiny in IVD degeneration (IVDD). However, its physiological and pathological roles in human NPSCs are unclear. In this study, we found that the content of ASIC1a increased with IVDD in both rats and human discs. In acidosis-treated NPSCs, the expression level of ASIC1a increased, accompanied by inhibition of cells viability and activation of mitochondrial apoptotic pathway. Additionally, ASIC1a overexpression activated the mitochondrial apoptotic pathway and increased the level of cellular and mitochondrial ROS in human NPSCs. Moreover, we demonstrated that the dysfunction of SIRT3-regulated mitochondrial redox homeostasis was involved in ASIC1a overexpression-induced apoptosis in human NPSCs. The in vivo experiments also demonstrated that the ASIC1a/SIRT3 pathway was involved in IVDD. Overall, these findings showed that ASIC1a disrupted mitochondrial function and aggravated mitochondrial oxidative stress by inhibiting the expression of SIRT3, which activated human NPSC apoptosis and aggravated IVDD. These findings provide new insights for the development of innovative treatment strategies for IVDD.HighlightsAcidosis inhibited human NPSCs activity and promoted apoptosis via mitochondria.ASIC1a promoted acidosis-induced apoptosis of human NPSCs.ASIC1a inhibited SIRT3 expression, aggravating mitochondrial oxidative stress.ASIC1a promoted IVDD via mitochondrial oxidative stress and apoptosis.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2504120"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239242/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584690","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

Synergistic effects of AgNPs and zileuton on PCOS via ferroptosis and inflammation mitigation. AgNPs和zileuton通过铁下垂和炎症缓解对PCOS的协同作用。

IF 5.2 2区生物学

Redox Report Pub Date : 2025-12-01 Epub Date: 2024-12-26 DOI: 10.1080/13510002.2024.2445398

Amira K Eltokhy, Rehab Ahmed Ahmed El-Shaer, Omnia Safwat El-Deeb, Eman E Farghal, Rowida Raafat Ibrahim, Rasha Elesawy, Marwa Mahmoud Awad, Radwa Ismail, Shaimaa M Motawea, Doaa Shatat, Yasser Mostafa Hafez, Hend Ahmed El Hanafy, Marwa Mohamed Atef

{"title":"Synergistic effects of AgNPs and zileuton on PCOS via ferroptosis and inflammation mitigation.","authors":"Amira K Eltokhy, Rehab Ahmed Ahmed El-Shaer, Omnia Safwat El-Deeb, Eman E Farghal, Rowida Raafat Ibrahim, Rasha Elesawy, Marwa Mahmoud Awad, Radwa Ismail, Shaimaa M Motawea, Doaa Shatat, Yasser Mostafa Hafez, Hend Ahmed El Hanafy, Marwa Mohamed Atef","doi":"10.1080/13510002.2024.2445398","DOIUrl":"https://doi.org/10.1080/13510002.2024.2445398","url":null,"abstract":"Background: The most prevalent endocrine disorder affecting women is PCOS. Programmed death of ovarian cells has yet to be elucidated. Ferroptosis is a kind of iron-dependent necrosis featured by significantly Fe+2-dependent lipid peroxidation. The ongoing study aimed to reinforce fertility by combining therapy with AgNPs and (Zileuton) in PCOS rats' model.Methods: The study included 75 adult female rats divided into 5 groups; control, PCOS, PCOS treated with AgNPs, PCOS treated with Zileuton, and PCOS group treated with AgNPs and Zileuton. The study investigated the anti-ferroptotic, anti-inflammatory, antioxidant, antiapoptotic, histopathological and immunohistochemical examinations of COX-2 and VEGF.Results: The combination of AgNPs and Zileuton showed significant reduction of inflammatory mediators (IL-6, TNF-α, NFk-B) compared with diseased group (P-value < 0.05), regression of ferroptosis marks (Panx1 and TLR4 expression, Fe+2 levels) compared with diseased group (P-value < 0.05), depression of apoptotic marker caspase 3 level compared with diseased animals (P-value < 0.05), depression of MDA level, elevation of HO-1, GPx4 activity, and reduction of Cox2 and VEGF as compared with the diseased, AgNPs or zileuton-treated groups (P-value < 0.05).Conclusion: The study showed that the combination of AgNPs and zileuton guards against, inflammation, apoptosis, and ferroptosis in PCO.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2445398"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142897257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","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}

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