{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T23:10:40Z","timestamp":1787008240261,"version":"build-2736575974"},"reference-count":47,"publisher":"SAGE Publications","issue":"5","license":[{"start":{"date-parts":[[2016,8,1]],"date-time":"2016-08-01T00:00:00Z","timestamp":1470009600000},"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":[[2016,8]]},"abstract":"<jats:p>\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Aims:<\/jats:italic>\n                    <\/jats:bold>\n                    Macrophages are of key importance for tissue repair after myocardial infarction (MI). Hydrogen sulfide (H\n                    <jats:sub>2<\/jats:sub>\n                    S) has been shown to exert cardioprotective effects in MI. However, the mechanisms by which H\n                    <jats:sub>2<\/jats:sub>\n                    S modulates cardiac remodeling and repair post-MI remain to be clarified.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Results:<\/jats:italic>\n                    <\/jats:bold>\n                    In our current study, we showed that H\n                    <jats:sub>2<\/jats:sub>\n                    S supplementation ameliorated pathological remodeling and dysfunction post-MI in wild-type (WT) and CSE KO mice, resulting in decreased infarct size and mortality, accompanied by an increase in the number of M2-polarized macrophages at the early stage of MI. Strikingly, adoptive transfer of NaHS-treated bone marrow-derived macrophages into WT and CSE KO mice with depleted macrophages also ameliorated MI-induced cardiac functional deterioration. Further mechanistic studies demonstrated that NaHS-induced M2 polarization was achieved by enhanced mitochondrial biogenesis and fatty acid oxidation.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Innovation and Conclusion:<\/jats:italic>\n                    <\/jats:bold>\n                    Our study shows (for the first time) that H\n                    <jats:sub>2<\/jats:sub>\n                    S may have the potential as a therapeutic agent for MI\n                    <jats:italic toggle=\"yes\">via<\/jats:italic>\n                    promotion of M2 macrophage polarization.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Rebound Track:<\/jats:italic>\n                    <\/jats:bold>\n                    This work was rejected during standard peer review and rescued by Rebound Peer Review (\n                    <jats:italic toggle=\"yes\">Antioxid Redox Signal<\/jats:italic>\n                    16:293\u2013296, 2012) with the following serving as open reviewers: Hideo Kimura, Chaoshu Tang, Xiaoli Tian, and Kenneth Olson.\n                    <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                    25, 268\u2013281.\n                  <\/jats:p>","DOI":"10.1089\/ars.2015.6577","type":"journal-article","created":{"date-parts":[[2016,6,13]],"date-time":"2016-06-13T22:20:39Z","timestamp":1465856439000},"page":"268-281","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":90,"title":["Hydrogen Sulfide Mitigates Myocardial Infarction\n                    <i>via<\/i>\n                    Promotion of Mitochondrial Biogenesis-Dependent M2 Polarization of Macrophages"],"prefix":"10.1177","volume":"25","author":[{"given":"Lei","family":"Miao","sequence":"first","affiliation":[{"name":"Fudan University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoyan","family":"Shen","sequence":"additional","affiliation":[{"name":"Fudan University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew","family":"Whiteman","sequence":"additional","affiliation":[{"name":"University of Exeter Medical School","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong","family":"Xin","sequence":"additional","affiliation":[{"name":"Fudan University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yaqi","family":"Shen","sequence":"additional","affiliation":[{"name":"Fudan University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoming","family":"Xin","sequence":"additional","affiliation":[{"name":"Fudan University","place":["China"]}],"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":"Yi-Zhun","family":"Zhu","sequence":"additional","affiliation":[{"name":"Fudan University","place":["China"]},{"name":"National University of Singapore","place":["Singapore"]},{"name":"School of Pharmacy, Macau University of Science and Technology, 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