{"title":"Vitamin C Enhances Anticancer Immunity","authors":"","doi":"10.20455/ros.2023.n811","DOIUrl":"https://doi.org/10.20455/ros.2023.n811","url":null,"abstract":"","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41563974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Phantom of the Oxygraph: Artifactual Oxygen Consumption Resulting from the Evolution of Nitrogen or Other Low Solubility Non-Oxygen Gas","authors":"","doi":"10.20455/ros.2023.c801","DOIUrl":"https://doi.org/10.20455/ros.2023.c801","url":null,"abstract":"","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45419394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The nuclear factor E2-related factor 2 (Nrf2) is best known for being the master transcriptional regulator of antioxidant genes. In addition, Nrf2 also regulates anti-inflammatory gene expression. Recent studies have discovered a critical function for Nrf2 signaling in modulating pain as well as in mediating the action of some commonly used non-steroidal anti-inflammatory and analgesic drugs (NSAIDs). This Cutting-Edge Research Highlights discusses these latest novel findings and proposes future research directions.
{"title":"Nrf2 Signaling in Modulating Pain and Inflammation","authors":"","doi":"10.20455/ros.2023.n807","DOIUrl":"https://doi.org/10.20455/ros.2023.n807","url":null,"abstract":"The nuclear factor E2-related factor 2 (Nrf2) is best known for being the master transcriptional regulator of antioxidant genes. In addition, Nrf2 also regulates anti-inflammatory gene expression. Recent studies have discovered a critical function for Nrf2 signaling in modulating pain as well as in mediating the action of some commonly used non-steroidal anti-inflammatory and analgesic drugs (NSAIDs). This Cutting-Edge Research Highlights discusses these latest novel findings and proposes future research directions.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41429007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Vitamin C for Offspring Pulmonary Protection from Maternal Smoking","authors":"","doi":"10.20455/ros.2023.n815","DOIUrl":"https://doi.org/10.20455/ros.2023.n815","url":null,"abstract":"","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46290536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Vitamin C: Novel Functions in Bone Homeostasis","authors":"","doi":"10.20455/ros.2023.n813","DOIUrl":"https://doi.org/10.20455/ros.2023.n813","url":null,"abstract":"","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44391753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The nuclear factor E2-related factor 1 (Nrf1 or NFE2L1) is a member of the CNC family of leucine zipper transcription factors, which also includes Nrf2, the most extensively studied transcriptional regulator of antioxidant genes. Like Nrf2, Nrf1 also regulates some antioxidant genes; however, it acts differently from Nrf2 in regulating many other cellular processes. This Cutting-Edge Research Highlights discusses some of the latest research findings on Nrf2 signaling in such biological processes as (1) cardiac regeneration, (2) GPx4-dependent ferroptosis, and (3) prolongevity. These advances have broadened the spectrum of Nrf1 physiological functions. (First online: February 25, 2023)
{"title":"Nrf1 (NFE2L1) Signaling in Homeostasis: Latest Advances","authors":"E. Ros","doi":"10.20455/ros.2023.n805","DOIUrl":"https://doi.org/10.20455/ros.2023.n805","url":null,"abstract":"The nuclear factor E2-related factor 1 (Nrf1 or NFE2L1) is a member of the CNC family of leucine zipper transcription factors, which also includes Nrf2, the most extensively studied transcriptional regulator of antioxidant genes. Like Nrf2, Nrf1 also regulates some antioxidant genes; however, it acts differently from Nrf2 in regulating many other cellular processes. This Cutting-Edge Research Highlights discusses some of the latest research findings on Nrf2 signaling in such biological processes as (1) cardiac regeneration, (2) GPx4-dependent ferroptosis, and (3) prolongevity. These advances have broadened the spectrum of Nrf1 physiological functions. \u0000(First online: February 25, 2023)","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45698937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
As of 2023, ROS will focus on two sections: (1) cutting-edge research highlights and (2) cutting-edge mini-reviews. The Journal will rarely publish original research contributions and will no longer consider lengthy review articles based primarily on research findings reported in scientific journals that lack a track record of high quality. In this editorial, the rationales for the 2023 new focus are provided along with a notion on how to define thorough mechanistic studies and prestigious journals. (First online: February 19, 2023)
{"title":"ROS 2023 New Focus: Cutting-Edge Research Highlights and Mini-Reviews","authors":"E. Ros","doi":"10.20455/ros.2023.e801","DOIUrl":"https://doi.org/10.20455/ros.2023.e801","url":null,"abstract":"As of 2023, ROS will focus on two sections: (1) cutting-edge research highlights and (2) cutting-edge mini-reviews. The Journal will rarely publish original research contributions and will no longer consider lengthy review articles based primarily on research findings reported in scientific journals that lack a track record of high quality. In this editorial, the rationales for the 2023 new focus are provided along with a notion on how to define thorough mechanistic studies and prestigious journals. \u0000(First online: February 19, 2023)","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42181794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Doxorubicin is among the most widely used anticancer drugs; however, its clinical use is associated with cardiomyopathy and heart failure. Studies show ferroptosis as a pivotal form of cell death underlying doxorubicin cardiomyopathy. Recently, multiple redox signaling pathways have been discovered to underly doxorubicin-induced ferroptosis. This Cutting-Edge Research Highlights discusses these latest advances, focusing on pathways involving Nrf2/HO-1, GPx4, and Alas1/heme synthesis. (First online: February 19, 2023) REFERENCES Zhu H, Sarkar S, Scott L, Danelisen I, Trush MA, Jia Z, et al. Doxorubicin Redox biology: redox cycling, topoisomerase inhibition, and oxidative stress. React Oxyg Species (Apex) 2016; 1(3):189–98. doi: https://dx.doi.org/10.20455/ros.2016.835 Higgins AY, O'Halloran TD, Chang JD. Chemotherapy-induced cardiomyopathy. Heart Fail Rev 2015; 20(6):721–30. doi: https://dx.doi.org/10.1007/s10741-015-9502-y Page RL, 2nd, O'Bryant CL, Cheng D, Dow TJ, Ky B, Stein CM, et al. Drugs that may cause or exacerbate heart failure: a scientific statement from the American Heart Association. Circulation 2016; 134(6):e32–69. doi: https://dx.doi.org/10.1161/CIR.0000000000000426 Fang X, Wang H, Han D, Xie E, Yang X, Wei J, et al. Ferroptosis as a target for protection against cardiomyopathy. Proc Natl Acad Sci USA 2019; 116(7):2672–80. doi: https://dx.doi.org/10.1073/pnas.1821022116 Dixon SJ, Lemberg KM, Lamprecht MR, Skouta R, Zaitsev EM, Gleason CE, et al. Ferroptosis: an iron-dependent form of nonapoptotic cell death. Cell 2012; 149(5):1060–72. doi: https://dx.doi.org/10.1016/j.cell.2012.03.042 Yang WS, Kim KJ, Gaschler MM, Patel M, Shchepinov MS, Stockwell BR. Peroxidation of polyunsaturated fatty acids by lipoxygenases drives ferroptosis. Proc Natl Acad Sci USA 2016; 113(34):E4966–75. doi: https://dx.doi.org/10.1073/pnas.1603244113 Kagan VE, Mao G, Qu F, Angeli JP, Doll S, Croix CS, et al. Oxidized arachidonic and adrenic PEs navigate cells to ferroptosis. Nat Chem Biol 2017; 13(1):81–90. doi: https://dx.doi.org/10.1038/nchembio.2238 Ichikawa Y, Ghanefar M, Bayeva M, Wu R, Khechaduri A, Naga Prasad SV, et al. Cardiotoxicity of doxorubicin is mediated through mitochondrial iron accumulation. J Clin Invest 2014; 124(2):617–30. doi: https://dx.doi.org/10.1172/JCI72931 Tadokoro T, Ikeda M, Ide T, Deguchi H, Ikeda S, Okabe K, et al. Mitochondria-dependent ferroptosis plays a pivotal role in doxorubicin cardiotoxicity. JCI Insight 2020; 5(9). doi: https://dx.doi.org/10.1172/jci.insight.132747 Abe K, Ikeda M, Ide T, Tadokoro T, Miyamoto HD, Furusawa S, et al. Doxorubicin causes ferroptosis and cardiotoxicity by intercalating into mitochondrial DNA and disrupting Alas1-dependent heme synthesis. Sci Signal 2022; 15(758):eabn8017. doi: https://dx.doi.org/10.1126/scisignal.abn8017
阿霉素是使用最广泛的抗癌药物之一;然而，其临床应用与心肌病和心力衰竭有关。研究表明，铁下垂是阿霉素心肌病细胞死亡的关键形式。最近，多种氧化还原信号通路被发现是阿霉素诱导铁下垂的基础。这篇前沿研究重点讨论了这些最新进展，重点是Nrf2/HO-1、GPx4和Alas1/血红素合成的途径。参考文献朱华，Sarkar S, Scott L, Danelisen I, Trush MA, Jia Z，等。氧化还原生物学:氧化还原循环、拓扑异构酶抑制和氧化应激。React oxygen Species (Apex) 2016;1(3): 189 - 98。doi: https://dx.doi.org/10.20455/ros.2016.835Higgins AY, O'Halloran TD, Chang JD。化疗所致心肌病。心力衰竭Rev 2015;20(6): 721 - 30。[doi: https://dx.doi.org/10.1007/s10741-015-9502-yPage RL, 2, O'Bryant CL, Cheng D, Dow TJ, Ky B, Stein CM，等。]可能导致或加剧心力衰竭的药物:美国心脏协会的一项科学声明。发行量2016;134 (6): e32 - 69。doi: https://dx.doi.org/10.1161/CIR.0000000000000426Fang X，王辉，韩东，谢娥，杨鑫，魏杰，等。上睑下垂作为预防心肌病的靶点。美国国家科学基金委2019;116(7): 2672 - 80。doi: https://dx.doi.org/10.1073/pnas.1821022116Dixon SJ, Lemberg KM, Lamprecht MR, Skouta R, Zaitsev EM, Gleason CE，等。铁下垂:一种非凋亡细胞死亡的铁依赖性形式。细胞2012;149(5): 1060 - 72。doi: https://dx.doi.org/10.1016/j.cell.2012.03.042Yang WS, Kim KJ, Gaschler MM, Patel M, Shchepinov MS, Stockwell BR。多不饱和脂肪酸过氧化脂氧合酶驱动铁下垂。2016;113 (34): e4966 - 75。氧化的花生四烯和肾上腺pe引导细胞铁下垂。生物化学学报，2017;13(1): 81 - 90。[doi: https://dx.doi.org/10.1038/nchembio.2238Ichikawa] Y, Ghanefar M, Bayeva M, Wu R, Khechaduri A, Naga Prasad SV等。阿霉素的心脏毒性是通过线粒体铁积累介导的。journal of clinical Invest 2014;124(2): 617 - 30。doi: https://dx.doi.org/10.1172/JCI72931Tadokoro T, Ikeda M, Ide T, Deguchi H, Ikeda S, Okabe K，等。线粒体依赖性铁下垂在阿霉素心脏毒性中起关键作用。JCI Insight 2020;5(9)。doi: https://dx.doi.org/10.1172/jci.insight.132747Abe K, Ikeda M, Ide T, Tadokoro T, Miyamoto HD, Furusawa S，等。阿霉素通过嵌入线粒体DNA和破坏alas1依赖性血红素合成引起铁中毒和心脏毒性。Sci Signal 2022;15 (758): eabn8017。doi: https://dx.doi.org/10.1126/scisignal.abn8017
{"title":"Redox Signaling in Doxorubicin-Induced Ferroptosis","authors":"E. Ros","doi":"10.20455/ros.2023.n803","DOIUrl":"https://doi.org/10.20455/ros.2023.n803","url":null,"abstract":"Doxorubicin is among the most widely used anticancer drugs; however, its clinical use is associated with cardiomyopathy and heart failure. Studies show ferroptosis as a pivotal form of cell death underlying doxorubicin cardiomyopathy. Recently, multiple redox signaling pathways have been discovered to underly doxorubicin-induced ferroptosis. This Cutting-Edge Research Highlights discusses these latest advances, focusing on pathways involving Nrf2/HO-1, GPx4, and Alas1/heme synthesis.\u0000(First online: February 19, 2023)\u0000REFERENCES \u0000\u0000Zhu H, Sarkar S, Scott L, Danelisen I, Trush MA, Jia Z, et al. Doxorubicin Redox biology: redox cycling, topoisomerase inhibition, and oxidative stress. React Oxyg Species (Apex) 2016; 1(3):189–98. doi: https://dx.doi.org/10.20455/ros.2016.835\u0000Higgins AY, O'Halloran TD, Chang JD. Chemotherapy-induced cardiomyopathy. Heart Fail Rev 2015; 20(6):721–30. doi: https://dx.doi.org/10.1007/s10741-015-9502-y\u0000Page RL, 2nd, O'Bryant CL, Cheng D, Dow TJ, Ky B, Stein CM, et al. Drugs that may cause or exacerbate heart failure: a scientific statement from the American Heart Association. Circulation 2016; 134(6):e32–69. doi: https://dx.doi.org/10.1161/CIR.0000000000000426\u0000Fang X, Wang H, Han D, Xie E, Yang X, Wei J, et al. Ferroptosis as a target for protection against cardiomyopathy. Proc Natl Acad Sci USA 2019; 116(7):2672–80. doi: https://dx.doi.org/10.1073/pnas.1821022116\u0000Dixon SJ, Lemberg KM, Lamprecht MR, Skouta R, Zaitsev EM, Gleason CE, et al. Ferroptosis: an iron-dependent form of nonapoptotic cell death. Cell 2012; 149(5):1060–72. doi: https://dx.doi.org/10.1016/j.cell.2012.03.042\u0000Yang WS, Kim KJ, Gaschler MM, Patel M, Shchepinov MS, Stockwell BR. Peroxidation of polyunsaturated fatty acids by lipoxygenases drives ferroptosis. Proc Natl Acad Sci USA 2016; 113(34):E4966–75. doi: https://dx.doi.org/10.1073/pnas.1603244113\u0000Kagan VE, Mao G, Qu F, Angeli JP, Doll S, Croix CS, et al. Oxidized arachidonic and adrenic PEs navigate cells to ferroptosis. Nat Chem Biol 2017; 13(1):81–90. doi: https://dx.doi.org/10.1038/nchembio.2238\u0000Ichikawa Y, Ghanefar M, Bayeva M, Wu R, Khechaduri A, Naga Prasad SV, et al. Cardiotoxicity of doxorubicin is mediated through mitochondrial iron accumulation. J Clin Invest 2014; 124(2):617–30. doi: https://dx.doi.org/10.1172/JCI72931\u0000Tadokoro T, Ikeda M, Ide T, Deguchi H, Ikeda S, Okabe K, et al. Mitochondria-dependent ferroptosis plays a pivotal role in doxorubicin cardiotoxicity. JCI Insight 2020; 5(9). doi: https://dx.doi.org/10.1172/jci.insight.132747\u0000Abe K, Ikeda M, Ide T, Tadokoro T, Miyamoto HD, Furusawa S, et al. Doxorubicin causes ferroptosis and cardiotoxicity by intercalating into mitochondrial DNA and disrupting Alas1-dependent heme synthesis. Sci Signal 2022; 15(758):eabn8017. doi: https://dx.doi.org/10.1126/scisignal.abn8017\u0000","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44222479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Metformin, a widely used antidiabetic drug, possesses other beneficial activities, including cardiovascular protection, anti-tumorigenesis, antiaging, and weight control. This Cutting-Edge Research Highlights outlines some latest basic research discoveries on metformin’s suppression of mitochondrial electron transport chain (METC) in the intervention of pulmonary inflammatory disorders, including tuberculosis and acute respiratory distress syndrome in animal models. These novel discoveries further support metformin as a pleiotropic drug for treating diverse diseases. (First online: February 19, 2023) REFERENCES Foretz M, Guigas B, Bertrand L, Pollak M, Viollet B. Metformin: from mechanisms of action to therapies. Cell Metab 2014; 20(6):953–66. doi: https://dx.doi.org/10.1016/j.cmet.2014.09.018 Vasan K, Werner M, Chandel NS. Mitochondrial metabolism as a target for cancer therapy. Cell Metab 2020; 32(3):341–52. doi: https://dx.doi.org/10.1016/j.cmet.2020.06.019 Kulkarni AS, Gubbi S, Barzilai N. Benefits of metformin in attenuating the hallmarks of aging. Cell Metab 2020; 32(1):15–30. doi: https://dx.doi.org/10.1016/j.cmet.2020.04.001 Day EA, Ford RJ, Smith BK, Mohammadi-Shemirani P, Morrow MR, Gutgesell RM, et al. Metformin-induced increases in GDF15 are important for suppressing appetite and promoting weight loss. Nat Metab 2019; 1(12):1202–8. doi: https://dx.doi.org/10.1038/s42255-019-0146-4 Coll AP, Chen M, Taskar P, Rimmington D, Patel S, Tadross JA, et al. GDF15 mediates the effects of metformin on body weight and energy balance. Nature 2020; 578(7795):444–8. doi: https://dx.doi.org/10.1038/s41586-019-1911-y Roca FJ, Whitworth LJ, Prag HA, Murphy MP, Ramakrishnan L. Tumor necrosis factor induces pathogenic mitochondrial ROS in tuberculosis through reverse electron transport. Science 2022; 376(6600):eabh2841. doi: https://dx.doi.org/10.1126/science.abh2841 Xian H, Liu Y, Rundberg Nilsson A, Gatchalian R, Crother TR, Tourtellotte WG, et al. Metformin inhibition of mitochondrial ATP and DNA synthesis abrogates NLRP3 inflammasome activation and pulmonary inflammation. Immunity 2021; 54(7):1463–77 e11. doi: https://dx.doi.org/10.1016/j.immuni.2021.05.004 Zhong Z, Liang S, Sanchez-Lopez E, He F, Shalapour S, Lin XJ, et al. New mitochondrial DNA synthesis enables NLRP3 inflammasome activation. Nature 2018; 560(7717):198–203. doi: https://dx.doi.org/10.1038/s41586-018-0372-z Billingham LK, Stoolman JS, Vasan K, Rodriguez AE, Poor TA, Szibor M, et al. Mitochondrial electron transport chain is necessary for NLRP3 inflammasome activation. Nat Immunol 2022; 23(5):692–704. doi: https://dx.doi.org/10.1038/s41590-022-01185-3 Guo H, Wang Q, Ghneim K, Wang L, Rampanelli E, Holley-Guthrie E, et al. Multi-omics analyses reveal that HIV-1 alters CD4+ T cell immunometabolism to fuel virus replication. Nat Immunol 2021; 22(4):423–33. doi: https://dx.doi.org/10.1038/s41590-021-00898-1
二甲双胍是一种广泛使用的降糖药，具有其他有益活性，包括心血管保护、抗肿瘤、抗衰老和控制体重。本前沿研究重点概述了二甲双胍抑制线粒体电子传递链(METC)干预肺部炎症性疾病(包括结核病和急性呼吸窘迫综合征)动物模型的一些最新基础研究发现。这些新发现进一步支持二甲双胍作为治疗多种疾病的多效性药物。[参考文献]foretz M, Guigas B, Bertrand L, Pollak M, Viollet B.二甲双胍:从作用机制到治疗。Cell Metab 2014;20(6): 953 - 66。doi: https://dx.doi.org/10.1016/j.cmet.2014.09.018Vasan K, Werner M, Chandel NS。线粒体代谢作为癌症治疗的靶点。Cell Metab 2020;32(3): 341 - 52。doi: https://dx.doi.org/10.1016/j.cmet.2020.06.019Kulkarni AS, Gubbi S, Barzilai N.二甲双胍在减缓衰老特征方面的益处。Cell Metab 2020;32(1): 15 - 30。doi: https://dx.doi.org/10.1016/j.cmet.2020.04.001Day EA, Ford RJ, Smith BK, Mohammadi-Shemirani P, Morrow MR, Gutgesell RM，等。二甲双胍诱导的GDF15增加对抑制食欲和促进体重减轻很重要。Nat Metab 2019;1(12): 1202 - 8。doi: https://dx.doi.org/10.1038/s42255-019-0146-4Coll AP, Chen M, Taskar P, Rimmington D, Patel S, Tadross JA，等。GDF15介导二甲双胍对体重和能量平衡的影响。自然2020;578(7795): 444 - 8。doi: https://dx.doi.org/10.1038/s41586-019-1911-yRoca FJ, Whitworth LJ, Prag HA, Murphy MP, Ramakrishnan L.肿瘤坏死因子通过反向电子传递诱导结核致病性线粒体ROS。科学2022;376 (6600): eabh2841。doi: https://dx.doi.org/10.1126/science.abh2841Xian H, Liu Y, Rundberg Nilsson A, Gatchalian R, Crother TR, Tourtellotte WG，等。二甲双胍抑制线粒体ATP和DNA合成可消除NLRP3炎性体激活和肺部炎症。免疫2021;e11 54(7): 1463 - 77。doi: https://dx.doi.org/10.1016/j.immuni.2021.05.004Zhong Z, Liang S, Sanchez-Lopez E, He F, Shalapour S，林晓军，等。新的线粒体DNA合成使NLRP3炎性体激活。自然2018;560(7717): 198 - 203。doi: https://dx.doi.org/10.1038/s41586-018-0372-zBillingham LK, Stoolman JS, Vasan K, Rodriguez AE, Poor TA, Szibor M，等。线粒体电子传递链是NLRP3炎性小体激活的必要条件。Nat Immunol 2022;23(5): 692 - 704。doi: https://dx.doi.org/10.1038/s41590-022-01185-3Guo H, Wang Q, Ghneim K, Wang L, Rampanelli E, Holley-Guthrie E，等。多组学分析表明，HIV-1改变CD4+ T细胞免疫代谢以促进病毒复制。Nat Immunol 2021;22(4): 423 - 33所示。doi: https://dx.doi.org/10.1038/s41590 - 021 - 00898 - 1
{"title":"Metformin, a “Wonder Drug”, Targets METC for Pulmonary Protection","authors":"E. Ros","doi":"10.20455/ros.2023.n801","DOIUrl":"https://doi.org/10.20455/ros.2023.n801","url":null,"abstract":"Metformin, a widely used antidiabetic drug, possesses other beneficial activities, including cardiovascular protection, anti-tumorigenesis, antiaging, and weight control. This Cutting-Edge Research Highlights outlines some latest basic research discoveries on metformin’s suppression of mitochondrial electron transport chain (METC) in the intervention of pulmonary inflammatory disorders, including tuberculosis and acute respiratory distress syndrome in animal models. These novel discoveries further support metformin as a pleiotropic drug for treating diverse diseases.\u0000(First online: February 19, 2023)\u0000REFERENCES\u0000\u0000Foretz M, Guigas B, Bertrand L, Pollak M, Viollet B. Metformin: from mechanisms of action to therapies. Cell Metab 2014; 20(6):953–66. doi: https://dx.doi.org/10.1016/j.cmet.2014.09.018\u0000Vasan K, Werner M, Chandel NS. Mitochondrial metabolism as a target for cancer therapy. Cell Metab 2020; 32(3):341–52. doi: https://dx.doi.org/10.1016/j.cmet.2020.06.019\u0000Kulkarni AS, Gubbi S, Barzilai N. Benefits of metformin in attenuating the hallmarks of aging. Cell Metab 2020; 32(1):15–30. doi: https://dx.doi.org/10.1016/j.cmet.2020.04.001\u0000Day EA, Ford RJ, Smith BK, Mohammadi-Shemirani P, Morrow MR, Gutgesell RM, et al. Metformin-induced increases in GDF15 are important for suppressing appetite and promoting weight loss. Nat Metab 2019; 1(12):1202–8. doi: https://dx.doi.org/10.1038/s42255-019-0146-4\u0000Coll AP, Chen M, Taskar P, Rimmington D, Patel S, Tadross JA, et al. GDF15 mediates the effects of metformin on body weight and energy balance. Nature 2020; 578(7795):444–8. doi: https://dx.doi.org/10.1038/s41586-019-1911-y\u0000Roca FJ, Whitworth LJ, Prag HA, Murphy MP, Ramakrishnan L. Tumor necrosis factor induces pathogenic mitochondrial ROS in tuberculosis through reverse electron transport. Science 2022; 376(6600):eabh2841. doi: https://dx.doi.org/10.1126/science.abh2841\u0000Xian H, Liu Y, Rundberg Nilsson A, Gatchalian R, Crother TR, Tourtellotte WG, et al. Metformin inhibition of mitochondrial ATP and DNA synthesis abrogates NLRP3 inflammasome activation and pulmonary inflammation. Immunity 2021; 54(7):1463–77 e11. doi: https://dx.doi.org/10.1016/j.immuni.2021.05.004\u0000Zhong Z, Liang S, Sanchez-Lopez E, He F, Shalapour S, Lin XJ, et al. New mitochondrial DNA synthesis enables NLRP3 inflammasome activation. Nature 2018; 560(7717):198–203. doi: https://dx.doi.org/10.1038/s41586-018-0372-z\u0000Billingham LK, Stoolman JS, Vasan K, Rodriguez AE, Poor TA, Szibor M, et al. Mitochondrial electron transport chain is necessary for NLRP3 inflammasome activation. Nat Immunol 2022; 23(5):692–704. doi: https://dx.doi.org/10.1038/s41590-022-01185-3\u0000Guo H, Wang Q, Ghneim K, Wang L, Rampanelli E, Holley-Guthrie E, et al. Multi-omics analyses reveal that HIV-1 alters CD4+ T cell immunometabolism to fuel virus replication. Nat Immunol 2021; 22(4):423–33. doi: https://dx.doi.org/10.1038/s41590-021-00898-1\u0000","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44426756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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