{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T06:09:49Z","timestamp":1779430189454,"version":"3.53.1"},"reference-count":53,"publisher":"SAGE Publications","issue":"6","license":[{"start":{"date-parts":[[2016,2,1]],"date-time":"2016-02-01T00:00:00Z","timestamp":1454284800000},"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":[[2016,2]]},"abstract":"<jats:p>\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Aim:<\/jats:italic>\n                    <\/jats:bold>\n                    Oxidative stress is a key contributor to endothelial dysfunction and associated cardiovascular pathogenesis. Hydrogen sulfide (H\n                    <jats:sub>2<\/jats:sub>\n                    S) is an antioxidant gasotransmitter that protects endothelial cells against oxidative stress. Sirtuin3 (SIRT3), which belongs to the silent information regulator 2 (SIR2) family, is an important deacetylase under oxidative stress. H\n                    <jats:sub>2<\/jats:sub>\n                    S is able to regulate the activity of several sirtuins. The present study aims to investigate the role of SIRT3 in the antioxidant effect of H\n                    <jats:sub>2<\/jats:sub>\n                    S in endothelial cells.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Results:<\/jats:italic>\n                    <\/jats:bold>\n                    Cultured EA.hy926 endothelial cells were exposed to hydrogen peroxide (H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    ) as a model of oxidative stress-induced cell injury. GYY4137, a slow-releasing H\n                    <jats:sub>2<\/jats:sub>\n                    S donor, improved cell viability, reduced oxidative stress and apoptosis, and improved mitochondrial function following H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    treatment. H\n                    <jats:sub>2<\/jats:sub>\n                    S reversed the stimulation of MAPK phosphorylation, downregulation of SIRT3 mRNA and reduction of the superoxide dismutase 2 and isocitrate dehydrogenase 2 expression which were induced by H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    . H\n                    <jats:sub>2<\/jats:sub>\n                    S also increased activator protein 1 (AP-1) binding activity with\n                    <jats:italic toggle=\"yes\">SIRT3<\/jats:italic>\n                    promoter and this effect was absent in the presence of the specific AP-1 inhibitor, SR11302 or curcumin. Paraquat administration to mice induced a defected endothelium-dependent aortic vasodilatation and increased oxidative stress in both mouse aorta and small mesenteric artery, which were alleviated by GYY4137 treatment. This vasoprotective effect of H\n                    <jats:sub>2<\/jats:sub>\n                    S was absent in\n                    <jats:italic toggle=\"yes\">SIRT3<\/jats:italic>\n                    knockout mice.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Innovation:<\/jats:italic>\n                    <\/jats:bold>\n                    The present results highlight a novel role for SIRT3 in the protective effect of H\n                    <jats:sub>2<\/jats:sub>\n                    S against oxidant damage in the endothelium both\n                    <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                    and\n                    <jats:italic toggle=\"yes\">in vivo.<\/jats:italic>\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Conclusion:<\/jats:italic>\n                    <\/jats:bold>\n                    H\n                    <jats:sub>2<\/jats:sub>\n                    S enhances AP-1 binding activity with the\n                    <jats:italic toggle=\"yes\">SIRT3<\/jats:italic>\n                    promoter, thereby upregulating SIRT3 expression and ultimately reducing oxidant-provoked vascular endothelial dysfunction.\n                    <jats:italic toggle=\"yes\">Antioxid. Redox Signal<\/jats:italic>\n                    . 24, 329\u2013343.\n                  <\/jats:p>","DOI":"10.1089\/ars.2015.6331","type":"journal-article","created":{"date-parts":[[2015,9,30]],"date-time":"2015-09-30T10:38:17Z","timestamp":1443609497000},"page":"329-343","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":103,"title":["SIRT3 Mediates the Antioxidant Effect of Hydrogen Sulfide in Endothelial Cells"],"prefix":"10.1177","volume":"24","author":[{"given":"Liping","family":"Xie","sequence":"first","affiliation":[{"name":"Nanjing Medical University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haihua","family":"Feng","sequence":"additional","affiliation":[{"name":"Nanjing Medical University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sha","family":"Li","sequence":"additional","affiliation":[{"name":"Nanjing Medical University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guoliang","family":"Meng","sequence":"additional","affiliation":[{"name":"Nanjing Medical University","place":["China"]},{"name":"Nantong University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shangmin","family":"Liu","sequence":"additional","affiliation":[{"name":"Nanjing Medical University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin","family":"Tang","sequence":"additional","affiliation":[{"name":"Nanjing Medical University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan","family":"Ma","sequence":"additional","affiliation":[{"name":"Nanjing Medical University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi","family":"Han","sequence":"additional","affiliation":[{"name":"the First Affiliated Hospital of Nanjing Medical University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yujiao","family":"Xiao","sequence":"additional","affiliation":[{"name":"Nanjing Medical University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yue","family":"Gu","sequence":"additional","affiliation":[{"name":"Nanjing Medical University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yongfeng","family":"Shao","sequence":"additional","affiliation":[{"name":"the First Affiliated Hospital of Nanjing Medical University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chung-Min","family":"Park","sequence":"additional","affiliation":[{"name":"Washington State University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ming","family":"Xian","sequence":"additional","affiliation":[{"name":"Washington State University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu","family":"Huang","sequence":"additional","affiliation":[{"name":"Chinese University of Hong Kong","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Albert","family":"Ferro","sequence":"additional","affiliation":[{"name":"King's College London","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rui","family":"Wang","sequence":"additional","affiliation":[{"name":"Lakehead University","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philip K.","family":"Moore","sequence":"additional","affiliation":[{"name":"National University of Singapore","place":["Singapore"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong","family":"Wang","sequence":"additional","affiliation":[{"name":"Temple University School of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yong","family":"Ji","sequence":"additional","affiliation":[{"name":"Nanjing Medical University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2016,2,20]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1042\/bse0520023"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1007\/s10059-009-0110-3"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.gene.2005.03.028"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/jre.12011"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.fct.2013.04.024"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1038\/embor.2011.65"},{"key":"e_1_3_3_8_2","first-page":"3460","article-title":"Hydrogen sulfide regulates vascular endoplasmic reticulum stress in apolipoprotein E knockout mice","volume":"124","author":"Chen ZF","year":"2011","unstructured":"Chen ZF, , Zhao B, , Tang XY, , Li W, , Zhu LL, , Tang CS, , DU JB, , and Jin HF. 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