{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T23:13:54Z","timestamp":1793142834585,"version":"4.5.0"},"reference-count":28,"publisher":"American Physiological Society","issue":"11","funder":[{"name":"Gifu University graduate School of Medicine"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2015,12,1]]},"abstract":"<jats:p> We investigated whether microRNA-145 (miR-145) has a cardioprotective effect in a rabbit model of myocardial infarction (MI) and in H9c2 rat cardiomyoblasts. Rabbits underwent 30 min of coronary occlusion, followed by 2 days or 2 wk of reperfusion. Control microRNA (control group; 2.5 nmol\/kg, n = 10) or miR-145 (miR-145 group, 2.5 nmol\/kg, n = 10) encapsulated in liposomes was intravenously administered immediately after the start of reperfusion. H9c2 rat cardiomyoblasts were transfected with miR-145. The MI size was significantly smaller in the miR-145 group than in the control group at 2 days and 2 wk post-MI. miR-145 had improved the cardiac function and remodeling at 2 wk post-MI. These effects were reversed by chloroquine. Western blot analysis showed that miR-145 accelerated the transition of LC3B I to II and downregulated p62\/SQSTM1 at 2 days or 2 wk after MI, but not at 4 wk, and activated Akt in the ischemic area at 2 days after MI. miR-145 inhibited the growth of H9c2 cells, accelerated the transition of LC3B I to II, and increased phosphorylated Akt in the H9c2 cells at 2 days after miR-145 transfection. Antagomir-145 significantly abolished the morphological change, the transition of LC3B I to II, and the increased phosphorylated Akt induced by miR-145 in H9c2 cells. We determined fibroblast growth factor receptor substrate 2 mRNA to be a target of miR-145, both in an in vivo model and in H9c2 cells. In conclusion, post-MI treatment with miR-145 protected the heart through the induction of cardiomyocyte autophagy by targeting fibroblast growth factor receptor substrate 2. <\/jats:p>","DOI":"10.1152\/ajpheart.00709.2014","type":"journal-article","created":{"date-parts":[[2015,10,3]],"date-time":"2015-10-03T00:23:26Z","timestamp":1443831806000},"page":"H1813-H1826","source":"Crossref","is-referenced-by-count":70,"title":["MicroRNA-145 repairs infarcted myocardium by accelerating cardiomyocyte autophagy"],"prefix":"10.1152","volume":"309","author":[{"given":"Kenshi","family":"Higashi","sequence":"first","affiliation":[{"name":"Department of Cardiology, Gifu University Graduate School of Medicine, Gifu, Japan; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshihisa","family":"Yamada","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Gifu University Graduate School of Medicine, Gifu, Japan; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shingo","family":"Minatoguchi","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Gifu University Graduate School of Medicine, Gifu, Japan; 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