{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,10]],"date-time":"2026-01-10T08:50:16Z","timestamp":1768035016836,"version":"3.49.0"},"reference-count":27,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2020,6,9]],"date-time":"2020-06-09T00:00:00Z","timestamp":1591660800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["analyticalsciencejournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cell Biochemistry &amp;amp; Function"],"published-print":{"date-parts":[[2020,12]]},"abstract":"<jats:p>Myocardial infarction (MI) leads to cardiac remodelling and heart failure. Cardiomyocyte apoptosis is considered a critical pathological phenomenon accompanying MI, but the pathogenesis mechanism remains to be explored. MicroRNAs (miRs), with the identity of negative regulator of gene expression, exist as an important contributor to apoptosis. During the experiment of this study, MI mice models were successfully established and sequencing data showed that the expression of miR\u201023a\u20105p was significantly enhanced during MI progression. Further steps were taken and it showed that apoptosis of cardiac cells weakened as miR\u201023a\u20105p was downregulated and on the contrary that apoptosis strengthened with the overexpression of miR\u201023a\u20105p. To explore its working mechanisms, bioinformatics analysis was conducted by referring to multi\u2010databases to predict the targets of miR\u201023a\u20105p. Further analysis suggested that those downstream genes enriched in several pathways, especially in the PI3K\/Akt singling pathway. Furthermore, it demonstrated that miR\u201023a\u20105p was negatively related to the phosphorylation of PI3K\/Akt, which plays a critical role in triggering cell apoptosis during MI. Recilisib\u2010activated PI3K\/Akt singling pathway could restrain apoptosis from inducing miR\u201023a\u20105p overexpression, and Miltefosine\u2010blocked PI3K\/Akt singling pathway could restrict apoptosis from inhibiting miR\u201023a\u20105p reduction. In conclusion, these findings revealed the pivotal role of miR\u201023a\u20105p\u2010PI3K\/Akt axis in regulating apoptosis during MI, introducing this novel axis as a potential indicator to detect ischemic heart disease and it could be used for therapeutic intervention.<\/jats:p>","DOI":"10.1002\/cbf.3536","type":"journal-article","created":{"date-parts":[[2020,6,10]],"date-time":"2020-06-10T01:37:01Z","timestamp":1591753021000},"page":"1047-1055","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Overexpression of <scp>microRNA<\/scp>\u201023a\u20105p induces myocardial infarction by promoting cardiomyocyte apoptosis through inhibited of <scp>PI3K<\/scp>\/<scp>AKT<\/scp> signalling pathway"],"prefix":"10.1002","volume":"38","author":[{"given":"Jiechun","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Cardiothoracic surgery Huashan Hospital of Fudan University  Shanghai 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