Redox Report最新文献

{"title":"Artemisinin protected human bronchial epithelial cells from amiodarone-induced oxidative damage via 5'-AMP-activated protein kinase (AMPK) activation.","authors":"Chao Yang, Wenjun Xiong, Jiayi Dong, Xia Zhao, Guang Liang, Wenhua Zheng","doi":"10.1080/13510002.2024.2447721","DOIUrl":"10.1080/13510002.2024.2447721","url":null,"abstract":"<p><strong>Background: </strong>Amiodarone, a common antiarrhythmic drug, is known for its severe side effects, including pulmonary toxicity, which involves oxidative stress and apoptosis. Artemisinin, an antimalarial drug, has shown cytoprotective properties by inhibiting oxidative stress and apoptosis. This study investigated the protective effects of artemisinin against amiodarone-induced toxicity in human bronchial epithelial cells (BEAS-2B) and mouse models.</p><p><strong>Results: </strong><i>In vitro</i> experiments revealed that amiodarone decreased cell viability, increased LDH release, ROS generation, caspase 3 activation, and apoptosis in BEAS-2B cells. Artemisinin counteracted these effects by upregulating p-AMPK, CaMKK2, Nrf2, and SOD1 protein levels, thereby protecting the cells from oxidative damage. The protective effect of artemisinin was diminished by the AMPK inhibitor Compound C or AMPKα knockdown. <i>In vivo</i> experiments demonstrated that artemisinin increased p-AMPK and Nrf2 protein levels in lung tissues, protecting against amiodarone-induced apoptosis and bronchial epithelial cell shedding in mice.</p><p><strong>Conclusion: </strong>These findings suggest that artemisinin protects airway epithelial cells and lung tissue from amiodarone-induced oxidative stress and apoptosis through AMPK activation, offering potential new strategies for preventing and treating amiodarone-induced pulmonary toxicity.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2447721"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11731350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142972170","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}

{"title":"Kaempferol protects against doxorubicin-induced myocardial damage by inhibiting mitochondrial ROS-dependent ferroptosis.","authors":"Lin Zhang, Xiaorui Liu, Juan Wang, Zimu Li, Siqi Wang, Wen Yang, Yang Hai, Dongling Liu","doi":"10.1080/13510002.2025.2503130","DOIUrl":"10.1080/13510002.2025.2503130","url":null,"abstract":"<p><strong>Background: </strong>Doxorubicin (DOX), a widely used chemotherapeutic agent, is limited in clinical application due to its dose-dependent cardiotoxicity. Therefore, it is crucial to explore alternative therapeutic molecules or drugs for mitigating DOX-induced cardiomyopathy (DIC). In this study aimed to explore underlying mechanisms of the cardioprotective effects of Kaempferol (KP) against DIC.</p><p><strong>Methods: </strong>H9c2 cell-based DIC model were established to explore the pharmacological mechanism. The levels of mitochondrial membrane potential, mitochondrial ROS, mitochondrial Fe²⁺ and lipid peroxidation were detected using JC-1, TMRE, Mito-SOX, Mito-Ferro Green and C11-BODIPY 581/591 probes. Furthermore, Western blot analysis measured the expression of key regulatory proteins, and NRF2-targeting siRNA was transfected into H9c2 cells. The nuclear translocation of NRF2 was assessed by immunofluorescence.</p><p><strong>Results: </strong>Data revealed that KP mitigated DOX-induced mitochondrial damage and ferroptosis via reducing membrane potential, mitochondrial ROS/Fe²⁺, and regulating lipid metabolism. Mechanistically, Western blot analysis revealed that KP inhibited DOX-induced ferroptosis by activating NRF2/SLC7A11/GPX4 axis. Moreover, KP promoted the accumulation and nuclear translocation of NRF2 protein.</p><p><strong>Conclusion: </strong>These findings demonstrated that KP protected against DOX-induced myocardial damage by inhibiting mitochondrial ROS-dependent ferroptosis. This provides novel insights into KP as a promising drug candidate for cardioprotection.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2503130"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12082743/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144027699","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}

{"title":"FASN regulates CSE-induced apoptosis, oxidative stress and mitochondrial damage in type 2 alveolar epithelial cells by regulating NRF2 expression and nuclear translocation.","authors":"Kun Yang, Guiyin Zhu, Tian Peng, Yi Cheng, Xuejun Guo","doi":"10.1080/13510002.2025.2550412","DOIUrl":"10.1080/13510002.2025.2550412","url":null,"abstract":"<p><p><b>ABSTRACT</b>Smoking is a major etiological factor in numerous chronic lung diseases. However, the precise underlying mechanisms remain incompletely elucidated. In this study, we investigated the effects of cigarette smoke extract (CSE) on mitochondrial oxidative phosphorylation (OXPHOS), mitochondrial structure, and the antioxidant regulator Nuclear factor erythroid 2-related factor 2 (NRF2) in a rat lung epithelial-T-antigen negative cell line (RLE-6TN), focusing on the associated molecular pathways. CSE exposure significantly reduced cell viability, induced oxidative-antioxidant imbalance, and disrupted OXPHOS complex subunit expression and mitochondrial ultrastructure. Furthermore, an increased BCL2-Associated X (BAX) / B-cell lymphoma/leukemia 2 (BCL2) ratio activated the intrinsic apoptosis pathway. NRF2 knockdown exacerbated CSE-induced mitochondrial damage and apoptosis. Co-immunoprecipitation (co-IP) analysis revealed a direct interaction between NRF2 and Fatty Acid Synthase (FASN). CSE treatment significantly reduced NRF2-FASN binding. Notably, FASN knockout amplified oxidative stress, exacerbated damage to OXPHOS and mitochondrial structure, and diminished NRF2 expression and nuclear translocation. Collectively, our findings demonstrate that CSE exposure impairs NRF2 expression and nuclear translocation by disrupting FASN expression and its interaction with FASN. This impairment leads to mitochondrial OXPHOS dysfunction, structural damage, and ultimately apoptosis. Our findings identify FASN as a potential therapeutic target for mitigating smoking-associated lung injury.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2550412"},"PeriodicalIF":7.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145192490","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}

{"title":"Therapeutic potential of EVs loaded with CB2 receptor agonist in spinal cord injury via the Nrf2/HO-1 pathway.","authors":"Imran Ibrahim Shaikh, Ramesh Bhandari, Shekhar Singh, Xu Zhu, Khawar Ali Shahzad, Chuxiao Shao, Liming Cheng, Jian Xiao","doi":"10.1080/13510002.2024.2420572","DOIUrl":"10.1080/13510002.2024.2420572","url":null,"abstract":"<p><strong>Background: </strong>Spinal cord injury (SCI) poses a challenge due to limited treatment options. Recently, the effect and mechanism of Exo-loaded cannabinoid receptor type 2 (CB2) agonist AM1241(Exo + AM1241) have been applied in other inflammatory diseases but not in SCI.</p><p><strong>Methods: </strong>The SCI model was set up using C57BL/6 mice, followed by the treatment of Exo, AM1241, and Exo + AM1241. We assessed the effects of the following treatments on motor function recovery using BMS, and evaluated histological changes, apoptosis activity, inflammation, and oxidative stress in the SCI mice model. Additionally, the effect of following treatments on spinal cord neural stem cells (NSCs) was evaluated under lipopolysaccharides (LPS) induced inflammatory and oxidative models and, glutamate (Gluts) induced cell apoptosis models.</p><p><strong>Result: </strong>Our results demonstrated that Exo + AM1241 treatment significantly improved motor function recovery, after SCI by decreasing proinflammatory cytokines, and suppressing astrocyte/microglia (GFAP/Iba1) activation in the injury zone. Additionally, this treatment reduces pro-apoptotic proteins (Bax and caspase 3), increases the levels of the anti-apoptotic protein Bcl-2, enhances antioxidant defenses by boosting SOD and GSH, and lowers oxidative stress markers such as MDA. It also activates the Nuclear factor erythroid-2 (Nrf2) related factor 2 signaling pathway, thereby enhancing tissue protection against damage and cell death.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2420572"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11520104/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142522850","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}

{"title":"Methane saline suppresses ferroptosis via the Nrf2/HO-1 signaling pathway to ameliorate intestinal ischemia-reperfusion injury.","authors":"Qingrui Fan, Hulin Chang, Lifei Tian, Bobo Zheng, Ruiting Liu, Zeyu Li","doi":"10.1080/13510002.2024.2373657","DOIUrl":"10.1080/13510002.2024.2373657","url":null,"abstract":"<p><strong>Objectives: </strong>Intestinal ischemia-reperfusion (I/R) injury is a multifactorial and complex clinical pathophysiological process. Current research indicates that the pathogenesis of intestinal I/R injury involves various mechanisms, including ferroptosis. Methane saline (MS) has been demonstrated to primarily exert anti-inflammatory and antioxidant effects in I/R injury. In this study, we mainly investigated the effect of MS on ferroptosis in intestinal I/R injury and determined its potential mechanism.</p><p><strong>Methods: </strong>In vivo and in vitro intestinal I/R injury models were established to validate the relationship between ferroptosis and intestinal I/R injury. MS treatment was applied to assess its impact on intestinal epithelial cell damage, intestinal barrier disruption, and ferroptosis.</p><p><strong>Results: </strong>MS treatment led to a reduction in I/R-induced intestinal epithelial cell damage and intestinal barrier disruption. Moreover, similar to treatment with ferroptosis inhibitors, MS treatment reduced ferroptosis in I/R, as indicated by a decrease in the levels of intracellular pro-ferroptosis factors, an increase in the levels of anti-ferroptosis factors, and alleviation of mitochondrial damage. Additionally, the expression of Nrf2/HO-1 was significantly increased after MS treatment. However, the intestinal protective and ferroptosis inhibitory effects of MS were diminished after the use of M385 to inhibit Nrf2 in mice or si-Nrf2 in Caco-2 cells.</p><p><strong>Discussion: </strong>We proved that intestinal I/R injury was mitigated by MS and that the underlying mechanism involved modulating the Nrf2/HO-1 signaling pathway to decrease ferroptosis. MS could be a promising treatment for intestinal I/R injury.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2373657"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11259071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141634359","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}

{"title":"Bilirubin regulates cell death type by alleviating macrophage mitochondrial dysfunction caused by cigarette smoke extract.","authors":"Jingjing Wei, Yuan Tian, Jinshu Wei, Meiqi Guan, Xiaoya Yu, Jianing Xie, Guoquan Fan","doi":"10.1080/13510002.2024.2382946","DOIUrl":"10.1080/13510002.2024.2382946","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the effects and mechanisms of bilirubin on mitochondrial function and type of macrophage cell death after exposure to cigarette smoke extract (CSE).</p><p><strong>Methods: </strong>RAW264.7 macrophages were treated with different concentrations of CSE and bilirubin solutions and divided into four groups: control, CSE, bilirubin, and bilirubin + CSE groups. The necrotic and apoptotic states of the macrophages were determined using an Annexin V-fluorescein 5-isothiocyanate/propidium iodide (FITC/PI) staining kit. Cytoplasmic NOD-like receptor family, pyrin domain containing 3 (NLRP3) expression in macrophages was detected by immunofluorescence and the levels of IL-1β and IL-18 in the supernatants of culture medium were detected by enzyme linked immunosorbent assay (ELISA) test. A JC-1 mitochondrial membrane potential detection kit was used to assess mitochondrial membrane damage and the adenosine triphosphate (ATP) assay kit was used to determine intracellular ATP levels. After the macrophages were stained with reactive oxygen species (ROS) specific dye, 2',7'-Dichlorodihydrofluorescein diacetate (DCFH-DA), the fluorescence intensity and proportion of ROS-positive macrophages were measured using flow cytometry.</p><p><strong>Results: </strong>We observed that compared with those of 0 μM (control group), concentrations of 5, 10, or 20 μΜ bilirubin significantly decreased cell viability, which was increased by bilirubin exposure below 1 μM. The effect of CSE on macrophage viability was concentration- and time-dependent. Bilirubin of 0.2 μM could alleviate the inhibition of macrophage viability caused by 5% CSE. In addition, bilirubin intervention could reduce the occurrence of necrosis and pyroptosis to a certain extent.</p><p><strong>Conclusions: </strong>CSE could cause mitochondrial dysfunction in macrophages, as demonstrated by a decrease in mitochondrial membrane potential and intracellular ATP levels and an increase in ROS production, while bilirubin could relieve mitochondrial dysfunction caused by CSE.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2382946"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11288206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141793361","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}

{"title":"Hyperoxia exposure induces ferroptosis and apoptosis by downregulating PLAGL2 and repressing HIF-1α/VEGF signaling pathway in newborn alveolar typeII epithelial cell.","authors":"Yuting Zhu, Hongmei Hou, Yawen Li, Yanyu Zhang, Yuanyuan Fang, Si Chen, Le Zhang, Weilai Jin, Yahui Zhou","doi":"10.1080/13510002.2024.2387465","DOIUrl":"10.1080/13510002.2024.2387465","url":null,"abstract":"<p><strong>Backgroud: </strong>Bronchopulmonary dysplasia (BPD) is one of the most important complications plaguing neonates and can lead to a variety of sequelae. the ability of the HIF-1α/VEGF signaling pathway to promote angiogenesis has an important role in neonatal lung development.</p><p><strong>Method: </strong>Newborn rats were exposed to 85% oxygen. The effects of hyperoxia exposure on Pleomorphic Adenoma Gene like-2 (PLAGL2) and the HIF-1α/VEGF pathway in rats lung tissue were assessed through immunofluorescence and Western Blot analysis. In cell experiments, PLAGL2 was upregulated, and the effects of hyperoxia and PLAGL2 on cell viability were evaluated using scratch assays, CCK-8 assays, and EDU staining. The role of upregulated PLAGL2 in the HIF-1α/VEGF pathway was determined by Western Blot and RT-PCR. Apoptosis and ferroptosis effects were determined through flow cytometry and viability assays.</p><p><strong>Results: </strong>Compared with the control group, the expression levels of PLAGL2, HIF-1α, VEGF, and SPC in lung tissues after 3, 7, and 14 days of hyperoxia exposure were all decreased. Furthermore, hyperoxia also inhibited the proliferation and motility of type II alveolar epithelial cells (AECII) and induced apoptosis in AECII. Upregulation of PLAGL2 restored the proliferation and motility of AECII and suppressed cell apoptosis and ferroptosis, while the HIF-1α/VEGF signaling pathway was also revived.</p><p><strong>Conclusions: </strong>We confirmed the positive role of PLAGL2 and HIF-1α/VEGF signaling pathway in promoting BPD in hyperoxia conditions, and provided a promising therapeutic targets.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2387465"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11302460/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141894144","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}

{"title":"Sarmentosin alleviates doxorubicin-induced cardiotoxicity and ferroptosis <i>via</i> the p62-Keap1-Nrf2 pathway.","authors":"Zhihui Lin, Chang Wu, Dongyan Song, Chenxi Zhu, Bosen Wu, Jie Wang, Yangjing Xue","doi":"10.1080/13510002.2024.2392329","DOIUrl":"10.1080/13510002.2024.2392329","url":null,"abstract":"<p><p>Doxorubicin (Dox) is extensively used as an antitumor agent, but its severe cardiotoxicity significantly limits its clinical use. Current treatments for Dox-induced cardiotoxicity are inadequate, necessitating alternative solutions. This study evaluated the effects of sarmentosin, a compound from Sedum sarmentosum, on Dox-induced cardiotoxicity and dysfunction. Sarmentosin was administered as a pretreatment to both mice and H9c2 cells before Dox exposure. Subsequently, markers of Dox-induced cardiotoxicity and ferroptosis in serum and cell supernatants were measured. Western blot analysis was utilized to detect levels of ferroptosis, oxidative stress, and autophagy proteins. Additionally, echocardiography, hematoxylin-eosin staining, ROS detection, and immunofluorescence techniques were employed to support our findings. Results demonstrated that sarmentosin significantly inhibited iron accumulation, lipid peroxidation, and oxidative stress, thereby reducing Dox-induced ferroptosis and cardiotoxicity in C57BL/6 mice and H9c2 cells. The mechanism involved the activation of autophagy and the Nrf2 signaling pathway. These findings suggest that sarmentosin may prevent Dox-induced cardiotoxicity by mitigating ferroptosis. The study underscores the potential of compounds like sarmentosin in treating Dox-induced cardiotoxicity.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2392329"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11332294/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141992473","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}

{"title":"Fluorescent probes for sensing peroxynitrite: biological applications.","authors":"Yan Yang, Jinting Shang, Yiyuan Xia, Yuran Gui","doi":"10.1080/13510002.2024.2430157","DOIUrl":"10.1080/13510002.2024.2430157","url":null,"abstract":"<p><p>Peroxynitrite (ONOO^-) is a quintessential reactive oxygen species (ROS) and reactive nitrogen species (RNS), renowned for its potent oxidizing and nitrifying capabilities. Under normal physiological conditions, a baseline level of ONOO^- is present within the body. However, its production escalates significantly in response to oxidative stress. ONOO^- is highly reactive with various biomolecules <i>in vivo</i>, particularly proteins, lipids, and nucleic acids, thereby playing a role in a spectrum of physiological and pathological processes, such as inflammation, cancer, neurodegenerative diseases, and cardiovascular diseases. Consequently, detecting ONOO^- <i>in vivo</i> is of paramount importance for understanding the etiology of various diseases and facilitating early diagnosis. Fluorescent probes have become a staple in the identification of biomolecules due to their ease of use, convenience, and superior sensitivity and specificity. This review highlights the recent advancements in the development of fluorescent probes for the detection of ONOO^- in diverse disease models and provides an in-depth examination of their design and application.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2430157"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11587728/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142710924","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}

{"title":"A reactive oxygen species-related signature predicts the prognosis and immunosuppressive microenvironment in gliomas.","authors":"Xia Shan, Ruoyu Huang, Kuanyu Wang, Pei Yang","doi":"10.1080/13510002.2024.2433396","DOIUrl":"10.1080/13510002.2024.2433396","url":null,"abstract":"<p><strong>Objective: </strong>Intracellular redox homeostasis is crucial for a series of physiological processes. Reactive oxygen species (ROS) play important roles in redox processes. ROS can maintain cell reproduction and survival at moderate levels while promoting the initiation and progression of tumors at high levels.</p><p><strong>Methods: </strong>Based on a comprehensive analysis of ROS-related gene expression profiles, we established a gene signature associated with ROS to explore its influence on prognosis and immune microenvironment in gliomas.</p><p><strong>Results: </strong>The ROS-related gene expression profile dichotomized patients into two groups with different clinicopathological features and prognoses. A 19-gene ROS-related signature was used to robustly predict prognosis in both training and validation datasets. Functional analysis indicated an association between ROS levels and the immune microenvironment. The expression of immune checkpoints and M2-type markers was upregulated in the high-risk group, which suggested the immunosuppressive function of ROS.</p><p><strong>Conclusion: </strong>ROS-related signature is an independent prognostic factor in gliomas and could potentially exert immunosuppressive effects on the tumor microenvironment.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2433396"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11610310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142751039","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}