{"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":" ","pages":""},"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}
{"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":"1 1","pages":""},"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":" ","pages":""},"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":" ","pages":""},"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}
{"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":" ","pages":""},"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}
{"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":" ","pages":""},"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}
{"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":" ","pages":""},"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}
{"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":" ","pages":""},"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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