Redox Biology最新文献

{"title":"Exquisite sensitivity of Polycystin-1 to H2O2 concentration in the endoplasmic reticulum","authors":"Elisa Speranza ,&nbsp;Ilaria Sorrentino ,&nbsp;Alessandra Boletta ,&nbsp;Roberto Sitia","doi":"10.1016/j.redox.2024.103486","DOIUrl":"10.1016/j.redox.2024.103486","url":null,"abstract":"<div><div>Aquaporin11 (AQP11) is an endoplasmic reticulum (ER) resident peroxiporin. It allows H₂O₂ transport from the lumen to the cytosol, guaranteeing redox homeostasis and signaling in and between the two organelles. Interestingly, <em>Aqp11</em>^{<em>−/−</em>} mice develop a fatal, early onset polycystic kidney disease (PKD) similar to Autosomal Dominant PKD, a condition frequently associated with mutations of polycystin-1 (PC-1) in human patients. Here we investigated the molecular mechanisms of AQP11-associated PKD. Using different cell models, we show that transient downregulation of AQP11 selectively prevents the biogenesis of overexpressed PC-1. Expression of catalase in the ER lumen rescues the phenotype, demonstrating a direct role of (H₂O₂)_ER in controlling the complex maturation of PC-1. Analysis of endogenous Pc-1 revealed an additional regulatory role at the pre-translational level. Taken together, our results show that AQP11 controls the complex biogenesis of PC-1 at multiple levels governing H₂O₂ intra and inter-organellar fluxes, with important implications in the pathogenesis and onset of PKD.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"80 ","pages":"Article 103486"},"PeriodicalIF":10.7,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763840/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142954092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apoptotic breast cancer cells after chemotherapy induce pro-tumour extracellular vesicles via LAP-competent macrophages","authors":"Qi Zhang ,&nbsp;Xiaodi Liu ,&nbsp;Qiuxia Wei ,&nbsp;Shiyu Xiong ,&nbsp;Wanrong Luo ,&nbsp;Yingshi zhou ,&nbsp;Jincheng Cao ,&nbsp;Xiaolin Xu ,&nbsp;Rongbin Liu ,&nbsp;Xinyu Tang ,&nbsp;Wenyue Zhang ,&nbsp;Baoming Luo","doi":"10.1016/j.redox.2024.103485","DOIUrl":"10.1016/j.redox.2024.103485","url":null,"abstract":"<div><div>Chemotherapy is important in the systemic therapy for breast cancer. However, after chemotherapy, the left living tumour cells are more progressive. There is an urgent need to study the underlying mechanism which is still unclear to further improve the therapeutic efficacy of chemotherapy in breast cancer. Here we find a pro-tumour effect of the apoptotic cells induced by the chemotherapy, which is mediated by a new subset of macrophages undergoing LC3-associated phagocytosis (LAP). By transferring exosomal S100A11 into the living tumour cells after chemotherapy, the macrophage exhibits a more pro-tumour phenotype than classic M2-type macrophages. Moreover, S100A11 binds to IFITM3, inducing Akt phosphorylation of living tumour cells after chemotherapy, which promotes tumour progression. Of note, Akt inhibitor can enhance the therapeutic effcicay of chemotherapy in breast cancer. This study provides a novel mechanistic link between tumour-associated macrophages and breast cancer, uncovering Akt as a potential therapeutic target to improve chemotherapy efficacy.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"80 ","pages":"Article 103485"},"PeriodicalIF":10.7,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142925331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Genome-wide transcriptional effects of deletions of sulphur metabolism genes in Drosophila melanogaster” [Redox Biol. 36 (2020) 101654]","authors":"O. Zatsepina ,&nbsp;D. Karpov ,&nbsp;L. Chuvakova ,&nbsp;A. Rezvykh ,&nbsp;S. Funikov ,&nbsp;S. Sorokina ,&nbsp;A. Zakluta ,&nbsp;D. Garbuz ,&nbsp;V. Shilova ,&nbsp;M. Evgen'ev","doi":"10.1016/j.redox.2024.103431","DOIUrl":"10.1016/j.redox.2024.103431","url":null,"abstract":"","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"Article 103431"},"PeriodicalIF":10.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671755/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142676700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Shank3 ameliorates neuronal injury after cerebral ischemia/reperfusion via inhibiting oxidative stress and inflammation” [Redox Biol. 69 (2024) 102983]","authors":"Hongchen Zhang ,&nbsp;Yuan Feng ,&nbsp;Yanfang Si ,&nbsp;Chuanhao Lu ,&nbsp;Juan Wang ,&nbsp;Shiquan Wang ,&nbsp;Liang Li ,&nbsp;Wenyu Xie ,&nbsp;Zheming Yue ,&nbsp;Jia Yong ,&nbsp;Shuhui Dai ,&nbsp;Lei Zhang ,&nbsp;Xia Li","doi":"10.1016/j.redox.2024.103432","DOIUrl":"10.1016/j.redox.2024.103432","url":null,"abstract":"","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"Article 103432"},"PeriodicalIF":10.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671758/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142688658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NOX2 in Alzheimer's and Parkinson's disease","authors":"Christopher M. Dustin ,&nbsp;Sruti S. Shiva ,&nbsp;Alberto Vazquez ,&nbsp;Anum Saeed ,&nbsp;Tharick Pascoal ,&nbsp;Eugenia Cifuentes-Pagano ,&nbsp;Patrick J. Pagano","doi":"10.1016/j.redox.2024.103433","DOIUrl":"10.1016/j.redox.2024.103433","url":null,"abstract":"<div><div>Alzheimer's Disease (AD), and related dementias, represent a growing concern for the worldwide population given the increased numbers of people of advanced age. Marked by significant degradation of neurological tissues and critical processes, in addition to more specific factors such as the presence of amyloid plaques and neurofibrillary tangles in AD, robust discussion is ongoing regarding the precise mechanisms by which these diseases arise. One of the major interests in recent years has been the contribution of reactive oxygen species (ROS) and, particularly, the contribution of the ROS-generating NADPH Oxidase proteins. NADPH Oxidase 2 (NOX2), the prototypical member of the family, represents a particularly interesting target for study given its close association with vascular and inflammatory processes in all tissues, including the brain, and the association of these processes with AD development and progression. In this review, we discuss the most relevant and recent work regarding the contribution of NOX2 to AD progression in neuronal, microglial, and cerebrovascular signaling. Furthermore, we will discuss the most promising NOX2-targeted therapeutics for potential AD management and treatment.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"Article 103433"},"PeriodicalIF":10.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142757282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of receptor-independent fluid-phase pinocytosis promotes foamy monocyte formation in atherosclerotic mice","authors":"WonMo Ahn ,&nbsp;Faith N. Burnett ,&nbsp;Kamila Wojnar-Lason ,&nbsp;Jaser Doja ,&nbsp;Amritha Sreekumar ,&nbsp;Pushpankur Ghoshal ,&nbsp;Bhupesh Singla ,&nbsp;Graydon Gonsalvez ,&nbsp;Ryan A. Harris ,&nbsp;Xiaoling Wang ,&nbsp;Joseph M. Miano ,&nbsp;Gábor Csányi","doi":"10.1016/j.redox.2024.103423","DOIUrl":"10.1016/j.redox.2024.103423","url":null,"abstract":"<div><div>Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of death worldwide. Clinical and experimental data demonstrated that circulating monocytes internalize plasma lipoproteins and become lipid-laden foamy cells in hypercholesterolemic subjects. This study was designed to identify the endocytic mechanisms responsible for foamy monocyte formation, perform functional and transcriptomic analysis of foamy and non-foamy monocytes relevant to ASCVD, and characterize specific monocyte subsets isolated from the circulation of normocholesterolemic controls and hypercholesterolemic patients. We hypothesized that activation of fluid-phase macropinocytosis contributes to foamy monocyte formation <em>in vitro</em> and in hypercholesterolemic mice <em>in vivo</em>. High resolution scanning electron microscopy (SEM) and quantification of FITC/TRITC-dextran internalization demonstrated macropinocytosis stimulation in human (THP-1) and <em>wild type</em> murine monocytes. Stimulation of macropinocytosis induced foamy monocyte formation in the presence of unmodified, native LDL (nLDL) and oxidized LDL (ox-LDL) <em>in vitro</em>. Genetic blockade of macropinocytosis (<em><strong>LysMCre</strong></em><em><strong>+</strong></em> <em>Nhe1</em>^<em>f/f</em>) inhibited foamy monocyte formation in hypercholesterolemic mice <em>in vivo</em> and attenuated monocyte adhesion to atherosclerotic aortas <em>ex vivo</em>. Mechanistic studies identified NADPH oxidase 2 (Nox2)-derived superoxide anion (O₂^⋅−) as an important downstream signaling molecule stimulating macropinocytosis in monocytes. qRT-PCR identified CD36 as a major scavenger receptor that increases in response to lipid loading in monocytes and deletion of CD36 (<em>Cd36</em>^−/−) inhibited foamy monocyte formation in hypercholesterolemic mice. Bulk RNA-sequencing characterized transcriptional differences between non-foamy and foamy monocytes versus macrophages. Finally, flow cytometry analysis of CD14 and CD16 expression demonstrated a significant increase in intermediate monocytes in hypercholesterolemic patients compared to normocholesterolemic controls. These results provide novel insights into the mechanisms of foamy monocyte formation and potentially identify new therapeutic targets for the treatment of atherosclerosis.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"Article 103423"},"PeriodicalIF":10.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142748378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “FBXL4 protects against HFpEF through Drp1-Mediated regulation of mitochondrial dynamics and the downstream SERCA2a” [Redox Biol. 70 (2024) 103081]","authors":"Miyesaier Abudureyimu ,&nbsp;Xuanming Luo ,&nbsp;Lingling Jiang ,&nbsp;Xuejuan Jin ,&nbsp;Cuizhen Pan ,&nbsp;Wei Yu ,&nbsp;Junbo Ge ,&nbsp;Yingmei Zhang ,&nbsp;Jun Ren","doi":"10.1016/j.redox.2024.103430","DOIUrl":"10.1016/j.redox.2024.103430","url":null,"abstract":"","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"Article 103430"},"PeriodicalIF":10.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Complement receptor 3 mediates NADPH oxidase activation and dopaminergic neurodegeneration through a Src-Erk-dependent pathway” [Redox Biol. 14 (2018) 250–260]","authors":"Liyan Hou ,&nbsp;Ke Wang ,&nbsp;Cong Zhang ,&nbsp;Fuqiang Sun ,&nbsp;Yuning Che ,&nbsp;Xiulan Zhao ,&nbsp;Dan Zhang ,&nbsp;Huihua Li ,&nbsp;Qingshan Wang","doi":"10.1016/j.redox.2024.103429","DOIUrl":"10.1016/j.redox.2024.103429","url":null,"abstract":"","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"Article 103429"},"PeriodicalIF":10.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671759/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142676617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"YAP1 preserves tubular mitochondrial quality control to mitigate diabetic kidney disease","authors":"Siyang Ye ,&nbsp;Meng Zhang ,&nbsp;Xunhua Zheng ,&nbsp;Suchun Li ,&nbsp;Yuting Fan ,&nbsp;Yiqin Wang ,&nbsp;Huajing Peng ,&nbsp;Sixiu Chen ,&nbsp;Jiayi Yang ,&nbsp;Li Tan ,&nbsp;Manhuai Zhang ,&nbsp;Peichen Xie ,&nbsp;Xiaoyan Li ,&nbsp;Ning Luo ,&nbsp;Zhipeng Wang ,&nbsp;Leigang Jin ,&nbsp;Xiaoping Wu ,&nbsp;Yong Pan ,&nbsp;Jinjin Fan ,&nbsp;Yi Zhou ,&nbsp;Wei Chen","doi":"10.1016/j.redox.2024.103435","DOIUrl":"10.1016/j.redox.2024.103435","url":null,"abstract":"<div><div>Renal tubule cells act as a primary site of injury in diabetic kidney disease (DKD), with dysfunctional mitochondrial quality control (MQC) closely associated with progressive kidney dysfunction in this context. Our investigation delves into the observed inactivation of yes-associated protein 1 (YAP1) and consequential dysregulation of MQC within renal tubule cells among DKD subjects through bioinformatic analysis of transcriptomics data from the Gene Expression Omnibus (GEO) dataset. Receiver operating characteristic curve analysis unequivocally underscores the robust diagnostic accuracy of YAP1 and MQC-related genes for DKD. Furthermore, we observed YAP1 inactivation, accompanied by perturbed MQC, within cultured tubule cells exposed to high glucose (HG) and palmitic acid (PA). This pattern was also evident in the tubulointerstitial compartment of kidney sections from biopsy-approved DKD patients. Additionally, renal tubule cell-specific <em>Yap1</em> deletion exacerbated kidney injury in diabetic mice. Mechanistically, <em>Yap1</em> deletion disrupted MQC, leading to mitochondrial aberrations in mitobiogenesis and mitophagy within tubule cells, ultimately culminating in histologic tubular injury. Notably, <em>Yap1</em> deletion-induced renal tubule injury promoted the secretion of C-X-C motif chemokine ligand 1 (CXCL1), potentially augmenting M1 macrophage infiltration within the renal microenvironment. These multifaceted events were significantly ameliorated by administrating the YAP1 activator XMU-MP-1 in DKD mice. Consistently, bioinformatic analysis of transcriptomics data from the GEO dataset revealed a noteworthy upregulation of tubule cells-derived chemokine CXCL1 associated with macrophage infiltration among DKD patients. Crucially, overexpression of YAP1 via adenovirus transfection sustained mitochondrial membrane potential, mtDNA copy number, oxygen consumption rate, and activity of mitochondrial respiratory chain complex, but attenuated mitochondrial ROS production, thereby maintaining MQC and subsequently suppressing CXCL1 generation within cultured tubule cells exposed to HG and PA. Collectively, our study establishes a pivotal role of tubule YAP1 inactivation-mediated MQC dysfunction in driving DKD progression, at least in part, facilitated by promoting M1 macrophage polarization through a paracrine-dependent mechanism.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"Article 103435"},"PeriodicalIF":10.7,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142721744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interplay between epigenetics, senescence and cellular redox metabolism in cancer and its therapeutic implications","authors":"Geoffrey Balamurli ,&nbsp;Angeline Qiu Xia Liew ,&nbsp;Wee Wei Tee ,&nbsp;Shazib Pervaiz","doi":"10.1016/j.redox.2024.103441","DOIUrl":"10.1016/j.redox.2024.103441","url":null,"abstract":"<div><div>There is accumulating evidence indicating a close crosstalk between key molecular events regulating cell growth and proliferation, which could profoundly impact carcinogenesis and its progression. Here we focus on reviewing observations highlighting the interplay between epigenetic modifications, irreversible cell cycle arrest or senescence, and cellular redox metabolism. Epigenetic alterations, such as DNA methylation and histone modifications, dynamically influence tumour transcriptome, thereby impacting tumour phenotype, survival, growth and spread. Interestingly, the acquisition of senescent phenotype can be triggered by epigenetic changes, acting as a double-edged sword via its ability to suppress tumorigenesis or by facilitating an inflammatory milieu conducive for cancer progression. Concurrently, an aberrant redox metabolism, which is a function of the balance between reactive oxygen species (ROS) generation and intracellular anti-oxidant defences, influences signalling cascades and genomic stability in cancer cells by serving as a critical link between epigenetics and senescence. Recognizing this intricate interconnection offers a nuanced perspective for therapeutic intervention by simultaneously targeting specific epigenetic modifications, modulating senescence dynamics, and restoring redox homeostasis.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"Article 103441"},"PeriodicalIF":10.7,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142721745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}