{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T22:29:27Z","timestamp":1792708167200,"version":"4.5.0"},"reference-count":56,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2016,11,1]],"date-time":"2016-11-01T00:00:00Z","timestamp":1477958400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100002858","name":"China Postdoctoral Science Foundation","doi-asserted-by":"publisher","award":["2016M603098"],"award-info":[{"award-number":["2016M603098"]}],"id":[{"id":"10.13039\/501100002858","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Pineal Research"],"published-print":{"date-parts":[[2017,1]]},"abstract":"Abstract<\/jats:title>\n \n Mitochondrial dysfunction leads to reactive oxygen species (\n ROS<\/jats:styled-content>\n ) overload, exacerbating injury in myocardial infarction (\n MI<\/jats:styled-content>\n ). As a receptor for translocases in the outer mitochondrial membrane (\n Tom<\/jats:styled-content>\n ) complex, Tom70 has an unknown function in\n MI<\/jats:styled-content>\n , including melatonin\u2010induced protection against\n MI<\/jats:styled-content>\n injury. We delivered specific small interfering\n RNA<\/jats:styled-content>\n s against Tom70 or lentivirus vectors carrying Tom70a sequences into the left ventricles of mice or to cultured neonatal murine ventricular myocytes (\n NMVM<\/jats:styled-content>\n s). At 48\u00a0h post\u2010transfection, the left anterior descending coronary arteries of mice were permanently ligated, while the\n NMVM<\/jats:styled-content>\n s underwent continuous hypoxia. At 24\u00a0h after ischemia\/hypoxia, oxidative stress was assessed by dihydroethidium and lucigenin\u2010enhanced luminescence, mitochondrial damage by transmission electron microscopy and\n ATP<\/jats:styled-content>\n content, and cell apoptosis by terminal deoxynucleotidyl transferase\n dUTP<\/jats:styled-content>\n nick\u2010end labeling and caspase\u20103 assay. At 4\u00a0weeks after ischemia, cardiac function and fibrosis were evaluated in mice by echocardiography and Masson's trichrome staining, respectively. Ischemic\/hypoxic insult reduced Tom70 expression in cardiomyocytes. Tom70 downregulation aggravated post\u2010\n MI<\/jats:styled-content>\n injury, with increased mitochondrial fragmentation and\n ROS<\/jats:styled-content>\n overload. In contrast, Tom70 upregulation alleviated post\u2010\n MI<\/jats:styled-content>\n injury, with improved mitochondrial integrity and decreased\n ROS<\/jats:styled-content>\n production.\n PGC<\/jats:styled-content>\n \u20101\u03b1\/Tom70 expression in ischemic myocardium was increased with melatonin alone, but not when combined with luzindole. Melatonin attenuated post\u2010\n MI<\/jats:styled-content>\n injury in control but not in Tom70\u2010deficient mice. N\u2010acetylcysteine (\n NAC<\/jats:styled-content>\n ) reversed the adverse effects of Tom70 deficiency in mitochondria and cardiomyocytes, but at a much higher concentration than melatonin. Our findings showed that Tom70 is essential for melatonin\u2010induced protection against post\u2010\n MI<\/jats:styled-content>\n injury, by breaking the cycle of mitochondrial impairment and\n ROS<\/jats:styled-content>\n generation.\n <\/jats:p>","DOI":"10.1111\/jpi.12371","type":"journal-article","created":{"date-parts":[[2016,10,12]],"date-time":"2016-10-12T15:57:47Z","timestamp":1476287867000},"source":"Crossref","is-referenced-by-count":70,"title":["Melatonin attenuates postmyocardial infarction injury via increasing Tom70 expression"],"prefix":"10.1111","volume":"62","author":[{"given":"Hai\u2010Feng","family":"Pei","sequence":"first","affiliation":[{"name":"Department of Cardiology Chengdu Military General Hospital Chengdu China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juan\u2010Ni","family":"Hou","sequence":"additional","affiliation":[{"name":"Department of Cardiology Chengdu Military General Hospital Chengdu 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