{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,6]],"date-time":"2026-11-06T21:31:52Z","timestamp":1794000712527,"version":"4.8.0"},"reference-count":27,"publisher":"Bentham Science Publishers Ltd.","issue":"2","content-domain":{"domain":["eurekaselect.com"],"crossmark-restriction":true},"short-container-title":["CNR"],"published-print":{"date-parts":[[2020,8,4]]},"abstract":"<jats:sec>\n<jats:title>Background:<\/jats:title>\n<jats:p>Myocardial Infarction (MI), a kind of heart deficiency, is the main cause\nof death and disability. Autophagy, a metabolic process for the degradation of damaged proteins or\norganelles, is important for cardiac functions and regulated by several miRNAs including miRNA-\n101. The aim of this research was to investigate the effects of miR-101 in myocardial infarctioninduced\ninjury and the related mechanisms.<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Methods:<\/jats:title>\n<jats:p>MI model was induced by ligation of the left coronary artery. The in vitro model was established\nby hypoxia-induced H9c2 cells (rat myocardial cells). The overexpression of miR-101\nwas achieved by transfection. The expression of associated proteins was analyzed by Western blotting.\nThe level of miR-101 was analyzed by reverse transcription-polymerase chain reaction (RTPCR).\nThe target genes for miR-101 and the target sites were analyzed by TargetScan.<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Results:<\/jats:title>\n<jats:p>The results showed that miR-101 was decreased in MI mice (P&lt;0.01). Autophagy and\napoptosis were increased in MI-induced injury (in vivo) and in hypoxia treated myocardial cells (in\nvitro) (P&lt;0.01). miR-101 overexpression inhibited the increase of autophagy and apoptosis in mice\nand myocardial cells (P&lt;0.01). DDIT4 was a target gene of miR-101 and expressed increasingly in\nMI-induced injury mice and hypoxia treated myocardial cells. miR-101 could negatively regulate\nthe expression of DDIT4.<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Conclusion:<\/jats:title>\n<jats:p>This research suggested that miR-101 attenuated- MI-induced injury by targeting\nDDIT4 to regulate autophagy, which indicated that miR-101 or DDIT4 may be potential therapeutic\ntargets for heart injury.<\/jats:p>\n<\/jats:sec>","DOI":"10.2174\/1567202617666200211113016","type":"journal-article","created":{"date-parts":[[2020,2,11]],"date-time":"2020-02-11T14:51:53Z","timestamp":1581432713000},"page":"123-130","update-policy":"https:\/\/doi.org\/10.2174\/bsp_crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["MiR-101 Attenuates Myocardial Infarction-induced Injury by Targeting DDIT4 to Regulate Autophagy"],"prefix":"10.2174","volume":"17","author":[{"given":"Qiulan","family":"Li","sequence":"first","affiliation":[{"name":"Department of Anesthesiology, The Affiliated Zhangjiagang Hospital of Soochow University, Zhangjiagang City, Jiangsu Province, 215600, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanping","family":"Gao","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, The Affiliated Zhangjiagang Hospital of Soochow University, Zhangjiagang City, Jiangsu Province, 215600, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, The Affiliated Zhangjiagang Hospital of Soochow University, Zhangjiagang City, Jiangsu Province, 215600, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5731-4164","authenticated-orcid":true,"given":"Qingzhe","family":"Jia","sequence":"additional","affiliation":[{"name":"Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing City, Jiangsu Province, 210029, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"965","reference":[{"key":"ref=1","doi-asserted-by":"publisher","author":"Thygesen,K.","unstructured":"Thygesen K, Alpert JS, Jaffe AS.;et al. 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