{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T04:32:21Z","timestamp":1790224341256,"version":"4.1.0"},"reference-count":57,"publisher":"SAGE Publications","issue":"17","license":[{"start":{"date-parts":[[2019,10,25]],"date-time":"2019-10-25T00:00:00Z","timestamp":1571961600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Antioxidants &amp; Redox Signaling"],"published-print":{"date-parts":[[2019,12]]},"abstract":"<jats:sec>\n                    <jats:title>Aims:<\/jats:title>\n                    <jats:p>\n                      Clinical use of cisplatin (Cisp), one of the most widely used, common, and effective chemotherapeutic agents, is limited by its side effects, particularly tubular injury-associated nephrotoxicity. Previous studies suggest that hydrogen sulfide (H\n                      <jats:sub>2<\/jats:sub>\n                      S) alleviates Cisp-induced acute kidney injury (AKI). However, the underlying mechanism remains largely unclear.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      A single intraperitoneal injection of Cisp is employed to induce AKI, and the mice exhibit severe kidney dysfunction and histological damage at day 4 after Cisp injection. Here, we reported that H\n                      <jats:sub>2<\/jats:sub>\n                      S alleviated Cisp-caused renal toxicity via SIRT3 activation and subsequent improvement of mitochondrial ATP production. Using a biotin-switch assay, we showed that H\n                      <jats:sub>2<\/jats:sub>\n                      S increased S-sulfhydration of SIRT3 and induced deacetylation of its target proteins (OPA1, ATP synthase \u03b2, and superoxide dismutase 2). These effects of H\n                      <jats:sub>2<\/jats:sub>\n                      S were associated with a reduction of mitochondrial fragmentation, an increase in ATP generation, and less oxidative injury. Notably, the S-sulfhydration of SIRT3 induced by H\n                      <jats:sub>2<\/jats:sub>\n                      S was abrogated when Cys256, Cys259, Cys280, and Cys283 residues on SIRT3 (two zinc finger domains) were mutated.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Innovation and Conclusion:<\/jats:title>\n                    <jats:p>\n                      Our data suggest that H\n                      <jats:sub>2<\/jats:sub>\n                      S attenuates Cisp-induced AKI by preventing mitochondrial dysfunction via SIRT3 sulfhydrylation.\n                      <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                      31, 1302\u20131319.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1089\/ars.2019.7728","type":"journal-article","created":{"date-parts":[[2019,6,20]],"date-time":"2019-06-20T06:59:10Z","timestamp":1561013950000},"page":"1302-1319","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":73,"title":["S-Sulfhydration of SIRT3 by Hydrogen Sulfide Attenuates Mitochondrial Dysfunction in Cisplatin-Induced Acute Kidney Injury"],"prefix":"10.1177","volume":"31","author":[{"given":"Yujia","family":"Yuan","sequence":"first","affiliation":[{"name":"Key Laboratory of Transplant Engineering and Immunology, NHFPC, West China Hospital, Sichuan University, Chengdu, China."},{"name":"Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lingling","family":"Zhu","sequence":"additional","affiliation":[{"name":"Key Laboratory of Transplant Engineering and Immunology, NHFPC, West China Hospital, Sichuan University, Chengdu, China."},{"name":"Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lan","family":"Li","sequence":"additional","affiliation":[{"name":"Key Laboratory of Transplant Engineering and Immunology, NHFPC, West China Hospital, Sichuan University, Chengdu, China."},{"name":"Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jingping","family":"Liu","sequence":"additional","affiliation":[{"name":"Key Laboratory of Transplant Engineering and Immunology, NHFPC, West China Hospital, Sichuan University, Chengdu, China."},{"name":"Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu, China."},{"name":"Center for Metabolic and Vascular Biology, School for Nutrition and Health Promotion, College of Health Solutions, Arizona State University, Scottsdale, Arizona."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Younan","family":"Chen","sequence":"additional","affiliation":[{"name":"Key Laboratory of Transplant Engineering and Immunology, NHFPC, West China Hospital, Sichuan University, Chengdu, China."},{"name":"Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jingqiu","family":"Cheng","sequence":"additional","affiliation":[{"name":"Key Laboratory of Transplant Engineering and Immunology, NHFPC, West China Hospital, Sichuan University, Chengdu, China."},{"name":"Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tianqing","family":"Peng","sequence":"additional","affiliation":[{"name":"Critical Illness Research, Lawson Health Research Institute, London Health Sciences Centre, London, Canada."},{"name":"Departments of Medicine and Pathology, University of Western Ontario, London, Canada."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanrong","family":"Lu","sequence":"additional","affiliation":[{"name":"Key Laboratory of Transplant Engineering and Immunology, NHFPC, West China Hospital, Sichuan University, Chengdu, China."},{"name":"Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu, China."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2019,10,25]]},"reference":[{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1097\/SHK.0000000000000478"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.1007\/s11845-015-1328-z"},{"key":"e_1_3_4_4_2","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.2013121351"},{"key":"e_1_3_4_5_2","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2017.7157"},{"key":"e_1_3_4_6_2","doi-asserted-by":"publisher","DOI":"10.1155\/2018\/6717212"},{"key":"e_1_3_4_7_2","doi-asserted-by":"publisher","DOI":"10.3109\/10715762.2015.1067806"},{"key":"e_1_3_4_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2015.10.013"},{"key":"e_1_3_4_9_2","doi-asserted-by":"publisher","DOI":"10.1038\/srep23882"},{"key":"e_1_3_4_10_2","first-page":"547","article-title":"Membrane transporters as mediators of cisplatin side-effects","volume":"34","author":"Ciarimboli G.","year":"2014","unstructured":"Ciarimboli G. Membrane transporters as mediators of cisplatin side-effects. Anticancer Res, 34: 547\u2013550, 2014.","journal-title":"Anticancer Res"},{"key":"e_1_3_4_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejphar.2014.07.025"},{"key":"e_1_3_4_12_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.117.310933"},{"key":"e_1_3_4_13_2","article-title":"Sulfhydrated sirtuin-1 increasing its deacetylation activity is an essential epigenetics mechanism of anti-atherogenesis by hydrogen sulfide","author":"Du C","year":"2018","unstructured":"Du C, , Lin X, , Xu W, , Zheng F, , Cai J, , Yang J, , Cui Q, , Tang C, , Cai J, , Xu G, , and Geng B. Sulfhydrated sirtuin-1 increasing its deacetylation activity is an essential epigenetics mechanism of anti-atherogenesis by hydrogen sulfide. 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Crystal structures of human SIRT3 displaying substrate-induced conformational changes. J Biol Chem 284, 2439, 4\u201324405, 2009.","journal-title":"J Biol Chem 284, 2439"},{"key":"e_1_3_4_27_2","first-page":"150","article-title":"Sodium hydrogen sulfide (NaHS) ameliorates alterations caused by cisplatin in filtration slit diaphragm and podocyte cytoskeletal in rat kidney","volume":"6","author":"Karimi A","year":"2017","unstructured":"Karimi A, , Absalan F, , Khorsandi L, , Valizadeh A, , and Mansouri E. Sodium hydrogen sulfide (NaHS) ameliorates alterations caused by cisplatin in filtration slit diaphragm and podocyte cytoskeletal in rat kidney. 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