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Echocardiography indicated that melatonin notably mitigated the adverse left ventricle remodeling and alleviated cardiac dysfunction in\n                    <jats:styled-content style=\"fixed-case\">DCM<\/jats:styled-content>\n                    . The mechanisms were attributed to increased autophagy, reduced apoptosis, and alleviated mitochondrial dysfunction. Furthermore, melatonin inhibited Mst1 phosphorylation and promoted Sirt3 expression in\n                    <jats:styled-content style=\"fixed-case\">DCM<\/jats:styled-content>\n                    . These results indicated that melatonin may exert its effects through Mst1\/Sirt3 signaling. To verify this hypothesis, a\n                    <jats:styled-content style=\"fixed-case\">DCM<\/jats:styled-content>\n                    model using Mst1 transgenic (Mst1 Tg) and Mst1 knockout (Mst1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) mice was constructed. As expected, melatonin increased autophagy, reduced apoptosis and improved mitochondrial biogenesis in Mst1 Tg mice subjected to\n                    <jats:styled-content style=\"fixed-case\">DCM<\/jats:styled-content>\n                    injury, while it had no effects on Mst1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. In addition, cultured neonatal mouse cardiomyocytes were subjected to simulated diabetes to probe the mechanisms involved. Melatonin administration promoted autophagic flux as demonstrated by elevated\n                    <jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>\n                    3\u2010\n                    <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n                    and lowered p62 expression in the presence of bafilomycin A1. The results suggest that melatonin alleviates cardiac remodeling and dysfunction in\n                    <jats:styled-content style=\"fixed-case\">DCM<\/jats:styled-content>\n                    by upregulating autophagy, limiting apoptosis, and modulating mitochondrial integrity and biogenesis. The mechanisms are associated with Mst1\/Sirt3 signaling.\n                  <\/jats:p>","DOI":"10.1111\/jpi.12418","type":"journal-article","created":{"date-parts":[[2017,5,8]],"date-time":"2017-05-08T03:55:37Z","timestamp":1494215737000},"source":"Crossref","is-referenced-by-count":159,"title":["EXPRESSION OF CONCERN: Melatonin protects against diabetic cardiomyopathy through Mst1\/Sirt3 signaling"],"prefix":"10.1111","volume":"63","author":[{"given":"Mingming","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Cardiology Tangdu Hospital Fourth Military Medical University  Xi'an China"},{"name":"Department of Cardiology Xijing Hospital Fourth Military Medical University  Xi'an China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Cardiology Xijing Hospital Fourth Military Medical University  Xi'an 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