{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T18:33:42Z","timestamp":1789065222006,"version":"build-2803163510"},"reference-count":19,"publisher":"Canadian Science Publishing","issue":"3","license":[{"start":{"date-parts":[[2018,6,1]],"date-time":"2018-06-01T00:00:00Z","timestamp":1527811200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":["cdnsciencepub.com"],"crossmark-restriction":false},"short-container-title":["Biochem. Cell Biol."],"published-print":{"date-parts":[[2018,6]]},"abstract":"<jats:p> Background: ischemia\u2013reperfusion (I\/R) is a consequence of restored blood supply after myocardial infarction. Myocardial I\/R injury can be alleviated by reducing autophagy in heart tissue. MicroRNA-34a (miR-34a) has been shown to regulate autophagy in a renal model of I\/R, but it is not known whether it can protect cardiac tissues from I\/R injury. This study investigated how miR-34a protects myocardial cells from I\/R injury by inhibiting autophagy via regulation of tumor necrosis factor \u03b1 (TNF\u03b1). Methods: we constructed an I\/R model in vivo using Langendorff perfusion, and we constructed an in vivo model by treating neonatal rat cardiomyocytes (NRCMs) with hypoxia\u2013reoxygenation (H\/R method). Transfected adenoviral-overexpressed miR-34a mimics and controlled NRCMs after H\/R. We analyzed cell viability using the MTT assay and a cell counting kit-8 (CCK-8) assay. Changes in the rate of apoptosis were detected by flow cytometry. We investigated the effect mechanisms of miR-34a with Western blot and luciferase assays. Results: miR-34a expression decreased after in vivo reperfusion of the myocardial cells and heart tissues of neonatal rats. MiR-34a reduced apoptosis of the NRCMs and autophagy levels, simultaneously, after H\/R injury. Further, miR-34a decreased the expression of Lc3-II and p62, indicating that miR-34a reduces myocardial I\/R injury by decreasing TNF\u03b1 expression. Conclusion: miR-34a can inhibit autophagy levels after I\/R by targeting TNF\u03b1, thereby reducing myocardial injury. <\/jats:p>","DOI":"10.1139\/bcb-2016-0158","type":"journal-article","created":{"date-parts":[[2017,5,25]],"date-time":"2017-05-25T21:34:01Z","timestamp":1495748041000},"page":"349-354","update-policy":"https:\/\/doi.org\/10.1139\/csp-crossmark-policy","source":"Crossref","is-referenced-by-count":38,"title":["MicroRNA-34a protects myocardial cells against ischemia\u2013reperfusion injury through inhibiting autophagy via regulating TNF\u03b1 expression"],"prefix":"10.1139","volume":"96","author":[{"given":"Haifeng","family":"Shao","sequence":"first","affiliation":[{"name":"Department of Cardiology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China."},{"name":"Department of Cardiology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lili","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Cardiology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China."},{"name":"Department of Cardiology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Cardiology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China."},{"name":"Department of Cardiology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bozan","family":"Tang","sequence":"additional","affiliation":[{"name":"Department of Cardiology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China."},{"name":"Department of Cardiology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Cardiology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China."},{"name":"Department of Cardiology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiang","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Cardiology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China."},{"name":"Department of Cardiology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"155","reference":[{"key":"refg1\/ref1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.19.1.163"},{"key":"refg2\/ref2","doi-asserted-by":"publisher","DOI":"10.1007\/s00418-010-0748-0"},{"key":"refg3\/ref3","first-page":"8786","volume":"8","author":"Hashmi S.","year":"2015","journal-title":"Int. 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