{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T18:55:40Z","timestamp":1778612140648,"version":"3.51.4"},"reference-count":26,"publisher":"Wiley","license":[{"start":{"date-parts":[[2021,12,7]],"date-time":"2021-12-07T00:00:00Z","timestamp":1638835200000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Disease Markers"],"published-print":{"date-parts":[[2021,12,7]]},"abstract":"<jats:p>Objective. The purpose of this study is to explore the regulating role of microRNA-383-5p (miR-383-5p) in oxidative stress after acute myocardial infarction (AMI) through AMPK pathway via phosphofructokinase muscle-type (PFKM). Methods. We established the AMI model, and the model mice were injected with miR-383-5p agomir to study the effect of miR-383-5p in AMPK signaling pathways. The target gene for miR-383-5p was reported to be PFKM, so we hypothesized that overexpression of miR-383-5p inhibits activation of the AMPK signaling pathway. Results. In this research, we found that overexpression of miR-383-5p decreases myocardial oxidative stress, myocardial apoptosis, the expression level of PFKM malondialdehyde (MDA), and reactive oxygen species (ROS) in the myocardial tissues after AMI, and finally, AMI-induced cardiac systolic and diastolic function could be improved.Conclusion. This study demonstrated that miR-383-5p could reduce the oxidative stress after AMI through AMPK signaling pathway by targeting PFKM.<\/jats:p>","DOI":"10.1155\/2021\/8587535","type":"journal-article","created":{"date-parts":[[2021,12,7]],"date-time":"2021-12-07T23:05:24Z","timestamp":1638918324000},"page":"1-9","source":"Crossref","is-referenced-by-count":7,"title":["MicroRNA-383-5p Regulates Oxidative Stress in Mice with Acute Myocardial Infarction through the AMPK Signaling Pathway via PFKM"],"prefix":"10.1155","volume":"2021","author":[{"given":"Linlin","family":"Gao","sequence":"first","affiliation":[{"name":"Department of Cardiovascular Medicine, Taizhou People\u2019s Hospital, Taizhou, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhongbao","family":"Ruan","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, Taizhou People\u2019s Hospital, Taizhou, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4157-3190","authenticated-orcid":true,"given":"Gecai","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, Taizhou People\u2019s Hospital, Taizhou, China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","reference":[{"key":"1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra072139"},{"key":"2","doi-asserted-by":"publisher","DOI":"10.1023\/B:MCBI.0000044370.20328.36"},{"key":"3","doi-asserted-by":"publisher","DOI":"10.1002\/sctm.18-0120"},{"key":"4","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(04)00045-5"},{"key":"5","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2014.01.050"},{"key":"6","doi-asserted-by":"publisher","DOI":"10.1042\/CS20130011"},{"key":"7","doi-asserted-by":"publisher","DOI":"10.3390\/ijms21124370"},{"key":"8","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkx029"},{"issue":"6","key":"9","first-page":"518","article-title":"miR-383 inhibits proliferation of granulosa cells by down-regulation of cell cycle-related proteins in mice","volume":"35","author":"Z. 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