Redox Biology最新文献

{"title":"Regulation of mitochondrial oxidative phosphorylation through tight control of cytochrome c oxidase in health and disease - Implications for ischemia/reperfusion injury, inflammatory diseases, diabetes, and cancer.","authors":"Lucynda Pham, Tasnim Arroum, Junmei Wan, Lauren Pavelich, Jamie Bell, Paul T Morse, Icksoo Lee, Lawrence I Grossman, Thomas H Sanderson, Moh H Malek, Maik Hüttemann","doi":"10.1016/j.redox.2024.103426","DOIUrl":"https://doi.org/10.1016/j.redox.2024.103426","url":null,"abstract":"<p><p>Mitochondria are essential to cellular function as they generate the majority of cellular ATP, mediated through oxidative phosphorylation, which couples proton pumping of the electron transport chain (ETC) to ATP production. The ETC generates an electrochemical gradient, known as the proton motive force, consisting of the mitochondrial membrane potential (ΔΨ_m, the major component in mammals) and ΔpH across the inner mitochondrial membrane. Both ATP production and reactive oxygen species (ROS) are linked to ΔΨ_m, and it has been shown that an imbalance in ΔΨ_m beyond the physiological optimal intermediate range results in excessive ROS production. The reaction of cytochrome c oxidase (COX) of the ETC with its small electron donor cytochrome c (Cytc) is the proposed rate-limiting step in mammals under physiological conditions. The rate at which this redox reaction occurs controls ΔΨ_m and thus ATP and ROS production. Multiple mechanisms are in place that regulate this reaction to meet the cell's energy demand and respond to acute stress. COX and Cytc have been shown to be regulated by all three main mechanisms, which we discuss in detail: allosteric regulation, tissue-specific isoforms, and post-translational modifications for which we provide a comprehensive catalog and discussion of their functional role with 55 and 50 identified phosphorylation and acetylation sites on COX, respectively. Disruption of these regulatory mechanisms has been found in several common human diseases, including stroke and myocardial infarction, inflammation including sepsis, and diabetes, where changes in COX or Cytc phosphorylation lead to mitochondrial dysfunction contributing to disease pathophysiology. Identification and subsequent targeting of the underlying signaling pathways holds clear promise for future interventions to improve human health. An example intervention is the recently discovered noninvasive COX-inhibitory infrared light therapy that holds promise to transform the current standard of clinical care in disease conditions where COX regulation has gone awry.</p>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"103426"},"PeriodicalIF":10.7,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681831","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}

{"title":"Time-restricted eating reveals a \"younger\" immune system and reshapes the intestinal microbiome in human.","authors":"Yiran Chen, Xi Li, Ming Yang, Chen Jia, Zhenghao He, Suqing Zhou, Pinglang Ruan, Yikun Wang, Congli Tang, Wenjing Pan, Hai Long, Ming Zhao, Liwei Lu, Weijun Peng, Arne Akbar, Irene Xy Wu, Song Li, Haijing Wu, Qianjin Lu","doi":"10.1016/j.redox.2024.103422","DOIUrl":"https://doi.org/10.1016/j.redox.2024.103422","url":null,"abstract":"<p><p>Time-restricted eating (TRE) has been shown to extent lifespans in drosophila and mouse models by affecting metabolic and anti-inflammatory activities. However, the effect of TRE on the human immune system, especially on immunosenescence, intestinal microbiome, and metabolism remains unclear. We conducted a 30-day 16:8 TRE single-arm clinical trial with 49 participants. Participants consumed daily meals from 9 a.m. to 5 p.m., provided by a nutrition canteen with a balanced, calorie-appropriate nutrition, which is designed by clinical nutritionists (ChiCTR2200058137). We monitored weight changes and weight-related parameters and focused on changes in the frequency of CD4⁺ senescent T cells, immune repertoire from peripheral blood, as well as serum metabolites and gut microbiota. We found that up to 95.9 % of subjects experienced sustained weight loss after TRE. The frequency of circulating senescent CD4⁺ T cells was decreased, while the frequency of Th1, Treg, Tfh-like, and B cells was increased. Regarding the immune repertoire, the proportions of T cell receptor alpha and beta chains were increased, whereas B cell receptor kappa and lambda chains were reduced. In addition, a reduced class switch recombination from immunoglobulin M (IgM) to immunoglobulin A (IgA) was observed. TRE upregulated the levels of anti-inflammatory and anti-aging serum metabolites named sphingosine-1-phosphate and prostaglandin-1. Additionally, several anti-inflammatory bacteria and probiotics were increased, such as Akkermansia and Rikenellaceae, and the composition of the gut microbiota tended to be \"younger\". Overall, TRE showed multiple anti-aging effects, which may help humans maintain a healthy lifestyle to stay \"young\". Clinical Trial Registration URL: https://www.chictr.org.cn/showproj.html?proj=159876.</p>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"103422"},"PeriodicalIF":10.7,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142676702","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}

{"title":"Deficiency of muscle-generated brain-derived neurotrophic factor causes inflammatory myopathy through reactive oxygen species-mediated necroptosis and pyroptosis","authors":"Brian Pak Shing Pang ,&nbsp;Elsie Chit Yu Iu ,&nbsp;Miaojia Hang ,&nbsp;Wing Suen Chan ,&nbsp;Margaret Chui Ling Tse ,&nbsp;Connie Tsz Ying Yeung ,&nbsp;Mingfu Wang ,&nbsp;Parco Ming Fai Siu ,&nbsp;Chi Wai Lee ,&nbsp;Keqiang Ye ,&nbsp;Ho So ,&nbsp;Chi Bun Chan","doi":"10.1016/j.redox.2024.103418","DOIUrl":"10.1016/j.redox.2024.103418","url":null,"abstract":"<div><div>Idiopathic inflammatory myopathy (commonly known as myositis) is a group of immune-related diseases characterized by muscle damage, weakness, and fatigue with unknown causes. Although overactivated innate immunity is a widely believed cause of myositis onset, the mechanism that provokes and maintains a high immune response in myositis patients is still unclear. This study aims to test if brain-derived neurotrophic factor (BDNF) deficiency <em>per se</em> is sufficient to cause myositis and determine its underlying mechanism. We found that ablating BDNF production in skeletal muscle is sufficient to trigger myositis development in mice. Muscle-specific <em>Bdnf</em> knockout (MBKO) mice displayed extensive myocyte necrosis, mononuclear cell infiltration, and myophagocytosis. In association with these damages, elevated production of pro-inflammatory cytokines such as interleukin (IL) 23, IL-1β, IL-18, and tumor necrosis factor α (TNFα) was found in the muscle of MBKO mice. Disruption of sarcolemma integrity was also detected in MBKO mice, which is a result of necroptosis executioner Mixed lineage kinase domain-like protein (MLKL) and pyroptosis executioner Gasdermin D (GSDMD) activation. Mechanistically, diminishing BDNF synthesis in myotubes enhances the accumulation of mitochondrial reactive oxygen species (mtROS), which sensitizes the cells towards TNFα-induced receptor-interacting protein kinase (RIPs) activation and promotes the formation of NLR family pyrin domain containing 3 (NLRP3)-containing inflammasome. BDNF deficiency-induced cell death could be alleviated by scavenging mtROS, suppressing the activity of GSDMD, or inhibiting receptor-interacting kinase 3 (RIP3). Similarly, supplementation of BDNF mimetics, suppression of RIP3 activity, increasing the intramyocellular antioxidant, or enhancing mitophagy ameliorated the myopathies of MBKO mice and improved their muscle strength. Together, our study demonstrates that insufficient BDNF production in mouse muscle causes the development of pathological features of myositis via enhancing oxidative stress, necroptosis, and pyroptosis in myofibers.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"Article 103418"},"PeriodicalIF":10.7,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142627153","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":"PRDM16 suppresses ferroptosis to protect against sepsis-associated acute kidney injury by targeting the NRF2/GPX4 axis","authors":"Qiang Zheng ,&nbsp;Jihong Xing ,&nbsp;Xiaozhou Li ,&nbsp;Xianming Tang ,&nbsp;Dongshan Zhang","doi":"10.1016/j.redox.2024.103417","DOIUrl":"10.1016/j.redox.2024.103417","url":null,"abstract":"<div><div>Acute kidney injury (AKI) constitutes a significant public health issue. Sepsis accounts for over 50 % of AKI cases in the ICU. Recent findings from our research indicated that the PRD1-BF1-RIZ1 homeodomain protein 16 (PRDM16) inhibited the progression of diabetic kidney disease (DKD). However, its precise role and regulatory mechanism in sepsis-induced AKI remain obscure. This study reveals that lipopolysaccharide (LPS) and cecum ligation and puncture (CLP) instigated PRDM16 expression in Boston University mouse proximal tubule (BUMPT) cells and mouse kidneys, respectively. Functionally, PRDM16 curtailed LPS-induced ferroptosis. Mechanistically, PRDM16 associates with the promoter regions of nuclear factor-erythroid 2-related factor-2 (NRF2) and augments its expression, subsequently enhancing glutathione peroxidase 4 (GPX4) expression. Additionally, PRDM16 directly engages with the promoter regions of GPX4, stimulating its expression. Notably, these observations were corroborated in human renal tubular epithelial (HK-2) cells. Furthermore, the ablation of PRDM16 from kidney proximal tubules in mice inhibited NRF2 and GPX4 expression, leading to decreased glutathione (GSH)/oxidized glutathione (GSSG) ratio, increased Fe²⁺ and reactive oxygen species (ROS) production, exacerbated ferroptosis, and AKI progression. Conversely, PRDM16 knock-in exhibited the opposite effects. Ultimately, adenovirus (ADV)-PRDM16 plasmid or poly (lactide-glycolide acid) (PLGA)-encapsulated formononetin not only mitigated sepsis-induced AKI but also alleviated liver, cardiac, and lung injury. In summary, PRDM16 inhibits ferroptosis via the NRF2/GPX4 axis or GPX4 to prevent sepsis-induced multi-organ injury, including AKI. PLGA-encapsulated formononetin presents a promising therapeutic approach.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"Article 103417"},"PeriodicalIF":10.7,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142644678","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":"A promising drug repurposing approach for Alzheimer's treatment: Givinostat improves cognitive behavior and pathological features in APP/PS1 mice.","authors":"Qi-Chao Gao, Ge-Liang Liu, Qi Wang, Sheng-Xiao Zhang, Zhi-Lin Ji, Zhao-Jun Wang, Mei-Na Wu, Qi Yu, Pei-Feng He","doi":"10.1016/j.redox.2024.103420","DOIUrl":"https://doi.org/10.1016/j.redox.2024.103420","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is the most common neurodegenerative disease, characterized by memory loss, speech and motor defects, personality changes, and psychological disorders. The exact cause of AD remains unclear. Current treatments focus on maintaining neurotransmitter levels or targeting β-amyloid (Aβ) protein, but these only alleviate symptoms and do not reverse the disease. Developing new drugs is time-consuming, costly, and has a high failure rate. Utilizing multi-omics for drug repositioning has emerged as a new strategy. Based on transcriptomic perturbation data of over 40,000 drugs in human cells from the LINCS-L1000 database, our study employed the Jaccard index and hypergeometric distribution test for reverse transcriptional feature matching analysis, identifying Givinostat as a potential treatment for AD. Our research found that Givinostat improved cognitive behavior and brain pathology in models and enhanced hippocampal synaptic plasticity. Transcriptome sequencing revealed increased expression of mitochondrial respiratory chain complex proteins in the brains of APP/PS1 mice after Givinostat treatment. Functionally, Givinostat restored mitochondrial membrane potential, reduced reactive oxygen species, and increased ATP content in Aβ-induced HT22 cells. Additionally, it improved mitochondrial morphology and quantity in the hippocampus of APP/PS1 mice and enhanced brain glucose metabolic activity. These effects are linked to Givinostat promoting mitochondrial biogenesis and improving mitochondrial function. In summary, Givinostat offers a promising new strategy for AD treatment by targeting mitochondrial dysfunction.</p>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"103420"},"PeriodicalIF":10.7,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692756","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}

{"title":"TXNIP regulates pulmonary inflammation induced by Asian sand dust","authors":"So-Won Pak ,&nbsp;Woong-Il Kim ,&nbsp;Se-Jin Lee ,&nbsp;Sin-Hyang Park ,&nbsp;Young-Kwon Cho ,&nbsp;Joong-Sun Kim ,&nbsp;Jong-Choon Kim ,&nbsp;Sung-Hwan Kim ,&nbsp;In-Sik Shin","doi":"10.1016/j.redox.2024.103421","DOIUrl":"10.1016/j.redox.2024.103421","url":null,"abstract":"<div><div>Asian sand dust (ASD), a seasonal dust storm originating from the deserts of China and Mongolia, affects Korea and Japan during the spring, carrying soil particles and a variety of biochemical components. Exposure to ASD has been associated with the onset and exacerbation of respiratory disorders, although the underlying mechanisms remain unclear. This study investigates ASD-induced pulmonary toxicity and its mechanistic pathways, focusing on the role of thioredoxin-interacting protein (TXNIP). Using TXNIP knock-out (KO) mice and adeno-associated virus (AAV)-mediated TXNIP overexpression transgenic mice, we explored how TXNIP modulates ASD-induced pulmonary inflammation. Mice were exposed to ASD via intranasal administration on days 1, 3, and 5 to induce inflammation. ASD exposure led to significant pulmonary inflammation, evidenced by increased inflammatory cell counts and elevated cytokine levels in bronchoalveolar lavage fluid, as well as heightened protein expression of the TXNIP/NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome. TXNIP KO mice exhibited attenuated airway inflammation and downregulation of the NLRP3 inflammasome compared to wild-type controls, while AAV-mediated TXNIP overexpression mice showed exacerbated inflammatory responses, including elevated NLRP3 inflammasome expression, compared to AAV-GFP controls. These findings suggest that TXNIP is a key regulator of ASD-induced pulmonary inflammation.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"Article 103421"},"PeriodicalIF":10.7,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142627159","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":"Reactivation of MAPK-SOX2 pathway confers ferroptosis sensitivity in KRASG12C inhibitor resistant tumors","authors":"Kai Wang ,&nbsp;Xin Zhang ,&nbsp;Yufei Fan ,&nbsp;Liang Zhou ,&nbsp;Yajun Duan ,&nbsp;Su Li ,&nbsp;Zhongkan Sun ,&nbsp;Chunqian Zhang ,&nbsp;Haoyu Yang ,&nbsp;Wenxiu Yuan ,&nbsp;Linyuan Peng ,&nbsp;Xiaoyu Ma ,&nbsp;Siliang Xiang ,&nbsp;Tianzhi Wang ,&nbsp;Mei Yang ,&nbsp;Zhenyuan Zhang ,&nbsp;Jiaxuan Wang ,&nbsp;Zhongyuan Wang ,&nbsp;Minxian Qian","doi":"10.1016/j.redox.2024.103419","DOIUrl":"10.1016/j.redox.2024.103419","url":null,"abstract":"<div><div>The clinical success of KRAS^G12C inhibitors (G12Ci) including AMG510 and MRTX849 is limited by the eventual development of acquired resistance. A novel and effective treatment to revert or target this resistance is urgent. To this end, we established G12Ci (AMG510 and MRTX849) resistant KRAS^G12C mutant cancer cell lines and screened with an FDA-approved drug library. We found the ferroptosis inducers including sorafenib and lapatinib stood out with an obvious growth inhibition in the G12Ci resistant cells. Mechanistically, the G12Ci resistant cells exhibited reactivation of MAPK signaling, which repressed SOX2-mediated expression of cystine transporter SLC7A11 and iron exporter SLC40A1. Consequently, the low intracellular GSH level but high iron content engendered hypersensitivity of these resistant tumors to ferroptosis inducers. Ectopic overexpression of SOX2 or SLC7A11 and SLC40A1 conferred resistance to ferroptosis in the G12Ci resistant cells. Ferroptosis induced by sulfasalazine (SAS) achieved obvious inhibition on the tumor growth of xenografts derived from AMG510-resistant KRAS^G12C-mutant cells. Collectively, our results suggest a novel therapeutic strategy to treat patients bearing G12Ci resistant cancers with ferroptosis inducers.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"Article 103419"},"PeriodicalIF":10.7,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142627155","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":"A mechanistic systems biology model of brain microvascular endothelial cell signaling reveals dynamic pathway-based therapeutic targets for brain ischemia","authors":"Geli Li ,&nbsp;Yuchen Ma ,&nbsp;Sujie Zhang ,&nbsp;Wen Lin ,&nbsp;Xinyi Yao ,&nbsp;Yating Zhou ,&nbsp;Yanyong Zhao ,&nbsp;Qi Rao ,&nbsp;Yuchen Qu ,&nbsp;Yuan Gao ,&nbsp;Lianmin Chen ,&nbsp;Yu Zhang ,&nbsp;Feng Han ,&nbsp;Meiling Sun ,&nbsp;Chen Zhao","doi":"10.1016/j.redox.2024.103415","DOIUrl":"10.1016/j.redox.2024.103415","url":null,"abstract":"<div><div>Ischemic stroke is a significant threat to human health. Currently, there is a lack of effective treatments for stroke, and progress in new neuron-centered drug target development is relatively slow. On the other hand, studies have demonstrated that brain microvascular endothelial cells (BMECs) are crucial components of the neurovascular unit and play pivotal roles in ischemic stroke progression. To better understand the complex multifaceted roles of BMECs in the regulation of ischemic stroke pathophysiology and facilitate BMEC-based drug target discovery, we utilized a transcriptomics-informed systems biology modeling approach and constructed a mechanism-based computational multipathway model to systematically investigate BMEC function and its modulatory potential. Extensive multilevel data regarding complex BMEC pathway signal transduction and biomarker expression under various pathophysiological conditions were used for quantitative model calibration and validation, and we generated dynamic BMEC phenotype maps in response to various stroke-related stimuli to identify potential determinants of BMEC fate under stress conditions. Through high-throughput model sensitivity analyses and virtual target perturbations in model-based single cells, our model predicted that targeting succinate could effectively reverse the detrimental cell phenotype of BMECs under oxygen and glucose deprivation/reoxygenation, a condition that mimics stroke pathogenesis, and we experimentally validated the utility of this new target in terms of regulating inflammatory factor production, free radical generation and tight junction protection <em>in vitro</em> and <em>in vivo</em>. Our work is the first that complementarily couples transcriptomic analysis with mechanistic systems-level pathway modeling in the study of BMEC function and endothelium-based therapeutic targets in ischemic stroke.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"Article 103415"},"PeriodicalIF":10.7,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142627151","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":"Bioenergetic shift and proteomic signature induced by lentiviral-transduction of GFP-based biosensors","authors":"Sarah Barakat ,&nbsp;Şeyma Çimen ,&nbsp;Seyed Mohammad Miri ,&nbsp;Emre Vatandaşlar ,&nbsp;Hayriye Ecem Yelkenci ,&nbsp;Alejandro San Martín ,&nbsp;Mustafa Çağlar Beker ,&nbsp;Kıvanç Kök ,&nbsp;Gürkan Öztürk ,&nbsp;Emrah Eroglu","doi":"10.1016/j.redox.2024.103416","DOIUrl":"10.1016/j.redox.2024.103416","url":null,"abstract":"<div><div>Fluorescent proteins (FPs) stand as pivotal tools extensively employed across diverse biological research endeavors in various model systems. However, long-standing concerns surround their use due to the numerous side effects associated with their expression. Recent investigations have brought to light the significance of hydrogen peroxide (H₂O₂) that is associated with the maturation process of green fluorescent protein (GFP) fluorophores. The structural and functional impairments associated with GFP expression are possibly linked to this amount of H₂O₂. In this study, we assess the impact of the GFP-based HyPer7 biosensor on cellular homeostasis and proteome changes, aiming to identify potential risks related to oxidative stress responses that potentially risks the application of such tools. Cells expressing genome-integrated HyPer7 demonstrated altered mitochondrial membrane potential (MMP), which was alleviated by the addition of antioxidants or culturing cells at physiological normoxia (5 kPa O₂). Additionally, HyPer7-expressing cells also exhibited significant impairment in mitochondrial oxidative respiration, suggesting broader mitochondrial dysfunction. Through untargeted proteomics analysis, we identified 26 proteins exhibiting differential expression in HyPer7-expressing cells compared to respective control cells. Functional annotation analysis showed that the list of the delineated proteins is associated with cellular responses to stress and the regulation of antioxidant mechanisms. Our findings underscore the significance of caution and validation in ensuring a thorough comprehension of cellular responses when using fluorescent protein-based tools, thereby enhancing the reliability of the results.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"78 ","pages":"Article 103416"},"PeriodicalIF":10.7,"publicationDate":"2024-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142592860","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 “Hyperoxia induces glucose metabolism reprogramming and intracellular acidification by suppressing MYC/MCT1 axis in lung cancer” [Redox Biol. 61 (2023) 102647]","authors":"Xiucheng Liu ,&nbsp;Hao Qin ,&nbsp;Li Zhang ,&nbsp;Caili Jia ,&nbsp;Zhixiang Chao ,&nbsp;Xichun Qin ,&nbsp;Hao Zhang ,&nbsp;Chang Chen","doi":"10.1016/j.redox.2024.103409","DOIUrl":"10.1016/j.redox.2024.103409","url":null,"abstract":"","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"77 ","pages":"Article 103409"},"PeriodicalIF":10.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142547104","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}