Redox Biology最新文献_第2页

Corrigendum to "Targeting GSS-mediated glutathione synthesis: 6-Met induces oxidative stress dependent apoptosis via triggering mitochondrial bioenergetics metabolism crisis and mTOR suppression in glioblastoma" [Redox Biol. 96 (2026) 104334]. “靶向gss介导的谷胱甘肽合成：6-Met通过触发线粒体生物能量代谢危机和mTOR抑制诱导氧化应激依赖的胶质母细胞瘤细胞凋亡”[氧化还原生物学报，96(2026):104334]。

IF 16.2 1区生物学

Redox Biology Pub Date : 2026-08-28 DOI: 10.1016/j.redox.2026.104372

Jianhu Lin, Hongfei Zhou, Nengfang Ma, Yang Chen, Qinbo Chen, Shengnan Han, Hailong Yang, Xiaolong Zhang, Fugen Shangguan

引用次数: 0

Redox and structural determinants of mitochondrial complex III inhibition by triphenylphosphonium-conjugated atovaquone analogs 三苯基膦偶联阿托伐酮类似物抑制线粒体复合体III的氧化还原和结构决定因素

IF 11.4 1区生物学

Redox Biology Pub Date : 2026-08-28 DOI: 10.1016/j.redox.2026.104370

Bruna Rafaela Pereira Resende, Gang Cheng, Gabriel Canard, Didier Siri, Vanessa Leone, Micael Hardy, Balaraman Kalyanaraman

{"title":"Redox and structural determinants of mitochondrial complex III inhibition by triphenylphosphonium-conjugated atovaquone analogs","authors":"Bruna Rafaela Pereira Resende, Gang Cheng, Gabriel Canard, Didier Siri, Vanessa Leone, Micael Hardy, Balaraman Kalyanaraman","doi":"10.1016/j.redox.2026.104370","DOIUrl":"https://doi.org/10.1016/j.redox.2026.104370","url":null,"abstract":"Growing evidence indicates that cancer cell mitochondria remain functional and represent attractive therapeutic targets. Mitochondria-targeted drug delivery commonly uses triphenylphosphonium (TPP<ce:sup loc=\"post\">+</ce:sup>)-conjugated compounds, which preferentially accumulate in cancer cell mitochondria because of their highly negative membrane potential. Many TPP<ce:sup loc=\"post\">+</ce:sup>-conjugated agents inhibit mitochondrial electron transport chain complexes I and II, suppressing mitochondrial respiration and cancer cell proliferation. Recent studies suggest that electron-withdrawing substituents, such as trifluoromethyl groups, on the TPP<ce:sup loc=\"post\">+</ce:sup> phenyl rings alter electron density around the phosphorus center, enhancing mitochondrial uncoupling activity and antiproliferative effects. To determine how TPP<ce:sup loc=\"post\">+</ce:sup> electronic substituents influence redox properties, mitochondrial complex III interactions, and biological activity, we used mitochondria-targeted atovaquone (<ce:bold>Mito-ATO</ce:bold>) as a model system.","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"28 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148885498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Exposure to TBBPA and polystyrene nanoplastics induces cardiac fibrosis via the activation of the ESR/H19/Wnt pathway. 暴露于TBBPA和聚苯乙烯纳米塑料通过激活ESR/H19/Wnt途径诱导心脏纤维化。

IF 16.2 1区生物学

Redox Biology Pub Date : 2026-08-28 DOI: 10.1016/j.redox.2026.104368

Xiang-Yu Pei, Xi-Ran Wang, Shao-Yan Liu, Meng-Die Cheng, Chang-Lei Li, Shuo Li, Hai-Ming Xu, Yin-Feng Zhang

{"title":"Exposure to TBBPA and polystyrene nanoplastics induces cardiac fibrosis via the activation of the ESR/H19/Wnt pathway.","authors":"Xiang-Yu Pei, Xi-Ran Wang, Shao-Yan Liu, Meng-Die Cheng, Chang-Lei Li, Shuo Li, Hai-Ming Xu, Yin-Feng Zhang","doi":"10.1016/j.redox.2026.104368","DOIUrl":"https://doi.org/10.1016/j.redox.2026.104368","url":null,"abstract":"Cardiac fibrosis is a key pathological driver of heart failure and cardiovascular mortality, with environmental pollutants being increasingly implicated. Tetrabromobisphenol A (TBBPA), a dominant brominated flame retardant (BFR), is environmentally pervasive and poses potential cardiotoxic risks. However, direct evidence for TBBPA-induced cardiac fibrosis in mammals is lacking. Additionally, its ability to adsorb onto nanoplastics, such as polystyrene (PS-NPs), raises concerns about combined toxicity, especially cardiotoxicity. To addressed this, we systematically evaluated the cardiotoxicity of TBBPA and PS-NPs in vivo and in vitro. In mice, environmentally relevant TBBPA exposure impaired cardiac function and induced inflammation and fibrosis, leading to cardiac remodeling, whereas co-exposure with PS-NPs only induced fibrosis. In H9C2 cells, TBBPA and PS-NPs individually promoted the expression of inflammatory, fibrotic, and hypertrophic markers, with co-exposure resulting in a synergistic exacerbation and a remodeling phenotype. Furthermore, transcriptomic and mechanistic data showed that ESR inhibitors blocked the H19/Wnt pathway activation induced by TBBPA or PS-NPs. Through gain- and loss-of-function experiments, we further confirmed that H19 mediates pollutant-induced Wnt/β-catenin activation and fibrotic responses, positioning H19 as a critical downstream mediator of the ESR/H19/Wnt axis. Overall, for the first time, this study elucidates the cardiotoxic profiles of TBBPA and PS-NPs and identifies the ESR/H19/Wnt axis as a key pro-fibrotic mechanism, highlighting a cardiovascular risk and a potential therapeutic target.","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"96 ","pages":"104368"},"PeriodicalIF":16.2,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148866587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Retraction notice to "FOXO3a-BAP1 axis regulates neuronal ferroptosis in early brain injury after subarachnoid hemorrhage" [Redox Biology 82 (2025) 103550]. “FOXO3a-BAP1轴调控蛛网膜下腔出血后早期脑损伤的神经元铁下垂”的回缩通知[Redox Biology 82(2025) 103550]。

IF 16.2 1区生物学

Redox Biology Pub Date : 2026-08-27 DOI: 10.1016/j.redox.2026.104356

Chengli Liu, Qi Tian, Zhijie Li, Guijun Wang, Wenrui Han, Shengming Jiang, Zhou Sun, Qingqing Xu, Long Wang, Jianming Liao, Mingchang Li

引用次数: 0

Retraction notice to "Corrigendum to 'Probucol ameliorates renal injury in diabetic nephropathy by inhibiting the expression of the redox enzyme p66Shc'" [Redox Biology 26 (2019) 101276]. “普布考通过抑制氧化还原酶p66Shc的表达改善糖尿病肾病肾损伤”的更正”[氧化还原生物学26(2019)101276]。

IF 16.2 1区生物学

Redox Biology Pub Date : 2026-08-27 DOI: 10.1016/j.redox.2026.104364

Shikun Yang, Li Zhao, Yachun Han, Yu Liu, Chao Chen, Ming Zhan, Xiaofen Xiong, Xuejing Zhu, Li Xiao, Chun Hu, Fuyou Liu, Zhiguang Zhou, Yashpal S Kanwar, Lin Sun

引用次数: 0

Retraction notice to "A novel compound DBZ ameliorates neuroinflammation in LPS-stimulated microglia and ischemic stroke rats: Role of Akt(Ser473)/GSK3β(Ser9)-mediated Nrf 2 activation" [Redox Biology 36 (2020) 101644]. “一种新型化合物DBZ改善lps刺激的小胶质细胞和缺血性卒中大鼠的神经炎症：Akt(Ser473)/GSK3β(Ser9)介导的Nrf 2激活的作用”[Redox Biology 36(2020) 101644]。

IF 16.2 1区生物学

Redox Biology Pub Date : 2026-08-27 DOI: 10.1016/j.redox.2026.104363

Sha Liao, Jingni Wu, Ruimin Liu, Shixiang Wang, Jing Luo, Yang Yang, Yannan Qin, Tao Li, Xiaopu Zheng, Jing Song, Xinfeng Zhao, Chaoni Xiao, Yajun Zhang, Liujiao Bian, Pu Jia, Yajun Bai, Xiaohui Zheng

引用次数: 0

Retraction notice to "Probucol ameliorates renal injury in diabetic nephropathy by inhibiting the expression of the redox enzyme p66Shc" [Redox Biol. 13 (2017) 482-497]. “普罗布考通过抑制氧化还原酶p66Shc的表达改善糖尿病肾病肾损伤”的撤回通知[氧化还原生物学杂志，13(2017)482-497]。

IF 16.2 1区生物学

Redox Biology Pub Date : 2026-08-27 DOI: 10.1016/j.redox.2026.104362

Shikun Yang, Li Zhao, Yachun Han, Yu Liu, Chao Chen, Ming Zhan, Xiaofen Xiong, Xuejing Zhu, Li Xiao, Chun Hu, Fuyou Liu, Zhiguang Zhou, Yashpal S Kanwar, Lin Sun

引用次数: 0

Cooperative inhibition of mTORC1 disrupts iron-redox homeostasis and triggers ferritinophagy-dependent ferroptosis in hepatocellular carcinoma. mTORC1的协同抑制破坏铁氧化还原稳态并引发肝细胞癌中铁蛋白吞噬依赖性铁凋亡。

IF 16.2 1区生物学

Redox Biology Pub Date : 2026-08-26 DOI: 10.1016/j.redox.2026.104369

Xinyu Chen, Zhen Tan, Shiqiao Zhao, Fan Li, Yilin Liu, Cong Ren, Jiaying Li, Hanghong Lo, Yue Cui, Aie Zhou, Chuanlin Zhu, Anguo Wu, Ning Jiang, Fang Ren

{"title":"Cooperative inhibition of mTORC1 disrupts iron-redox homeostasis and triggers ferritinophagy-dependent ferroptosis in hepatocellular carcinoma.","authors":"Xinyu Chen, Zhen Tan, Shiqiao Zhao, Fan Li, Yilin Liu, Cong Ren, Jiaying Li, Hanghong Lo, Yue Cui, Aie Zhou, Chuanlin Zhu, Anguo Wu, Ning Jiang, Fang Ren","doi":"10.1016/j.redox.2026.104369","DOIUrl":"https://doi.org/10.1016/j.redox.2026.104369","url":null,"abstract":"Hepatocellular carcinoma (HCC) remains a leading cause of cancer mortality, and the clinical utility of β-lapachone (β-Lap) is limited by dose-dependent toxicity. Here, we identify cryptotanshinone (CPT), a bioactive compound derived from Salvia miltiorrhiza, as a synergistic partner that enables dose reduction while enhancing antitumor efficacy. Integrated transcriptomic profiling, biochemical analyses, target engagement assays, and in vivo validation support that β-Lap and CPT cooperatively induce ferroptosis through disruption of iron-redox homeostasis. Mechanistically, β-Lap and CPT engage Raptor and mTOR, respectively, in vitro, supporting a model wherein their cooperative action leads to dual suppression of mTORC1 signaling. mTORC1 inhibition activates NCOA4-mediated ferritinophagy, promoting ferritin degradation and expansion of the labile Fe2+ pool. The consequent iron-dependent Fenton reaction drives excessive reactive oxygen species (ROS) accumulation and lipid peroxidation, culminating in ferroptotic cell death. Notably, this process occurs without downregulation of the canonical GPX4-SLC7A11 axis, defining a non-canonical, iron-amplified ferroptosis pathway. In xenograft models, the combination therapy significantly suppressed tumor growth without detectable systemic toxicity and recapitulated the molecular hallmarks observed in vitro, including mTORC1 inhibition, enhanced ferritinophagy, iron overload, and lipid peroxidation. Collectively, our findings support cooperative mTORC1 inhibition as a strategy to trigger ferritinophagy-dependent iron-redox collapse and non-canonical ferroptosis, providing a mechanistically informed and low-toxicity therapeutic approach for HCC.","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"97 ","pages":"104369"},"PeriodicalIF":16.2,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148881424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Crosstalk Between Cysteine and Lysine Modifications: Integrating Redox and Metabolic Regulation 半胱氨酸和赖氨酸修饰之间的串扰：整合氧化还原和代谢调节

IF 11.4 1区生物学

Redox Biology Pub Date : 2026-08-22 DOI: 10.1016/j.redox.2026.104357

Emily C. Mitchem, James R. Roede, Kristofer S. Fritz

{"title":"Crosstalk Between Cysteine and Lysine Modifications: Integrating Redox and Metabolic Regulation","authors":"Emily C. Mitchem, James R. Roede, Kristofer S. Fritz","doi":"10.1016/j.redox.2026.104357","DOIUrl":"https://doi.org/10.1016/j.redox.2026.104357","url":null,"abstract":"Protein post-translational modifications (PTMs) on amino acid residues enable dynamic cellular responses to changes in metabolic and redox state. Cysteine and lysine are among the most extensively modified amino acid residues, with both undergoing a diversity of acylation and oxidative modifications. Indeed, proximal (<10Å) cysteine and lysine residues may form integration nodes for crosstalk between metabolism and redox homeostasis pathways. This review highlights the interaction of proximal Cys-Lys residues, including influence on residue pKa by local electrostatics, cysteine-to-lysine transfer of PTM moieties, and covalent crosslinking. We discuss candidate Cys-Lys regulatory pairs in proteins involved in redox regulation, proteostasis, metabolic adaptation and inflammation. We further utilize computational modeling to identify proximity between cysteine and lysine residues in proteins known to be regulated by acylation and oxidative PTMs, and to demonstrate changes in these distances and local electrostatic potential due to lysine acetylation. Finally, we review how mass spectrometry-based proteomics and machine-learning PTM predictive tools can enable the identification, validation, and interpretation of proximal Cys-Lys interactions that regulate cellular responses to oxidative challenge and metabolic flux.","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"35 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2026-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148853195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Corrigendum to “Trem2 mediated Syk-dependent ROS amplification is essential for osteoclastogenesis in periodontitis microenvironment” [Redox Biol. 40 (2021) 101849] “Trem2介导的syk依赖性ROS扩增对于牙周炎微环境中的破骨细胞生成至关重要”的更正[Redox Biol. 40 (2021) 101849]

IF 11.4 1区生物学

Redox Biology Pub Date : 2026-08-04 DOI: 10.1016/j.redox.2026.104332

Yuteng Weng, Haicheng Wang, Lin Li, Yanhuizhi Feng, Shuyu Xu, Zuolin Wang

引用次数: 0