{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T20:33:52Z","timestamp":1785270832812,"version":"3.55.0"},"reference-count":29,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2024,1,6]],"date-time":"2024-01-06T00:00:00Z","timestamp":1704499200000},"content-version":"vor","delay-in-days":5,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["32160205"],"award-info":[{"award-number":["32160205"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Gene Medicine"],"published-print":{"date-parts":[[2024,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>The induction of cardiomyocyte (CM) proliferation is a promising approach for cardiac regeneration following myocardial injury. MicroRNAs (miRNAs) have been reported to regulate CM proliferation. In particular, miR\u2010431 expression decreases during cardiac development, according to Gene Expression Omnibus (GEO) microarray data. However, whether miR\u2010431 regulates CM proliferation has not been thoroughly investigated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We used integrated bioinformatics analysis of GEO datasets to identify the most significantly differentially expressed miRNAs. Real\u2010time quantitative PCR and fluorescence <jats:italic>in situ<\/jats:italic> hybridization were performed to determine the miRNA expression patterns in hearts. Gain\u2010 and loss\u2010of\u2010function assays were conducted to detect the role of miRNA in CM proliferation. Additionally, we detected whether miR\u2010431 affected CM proliferation in a myocardial infarction model. The TargetScan, miRDB and miRWalk online databases were used to predict the potential target genes of miRNAs. Luciferase reporter assays were used to study miRNA interactions with the targeting mRNA.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>First, we found a significant reduction in miR\u2010431 levels during cardiac development. Then, by overexpression and inhibition of miR\u2010431, we demonstrated that miR\u2010431 promotes CM proliferation <jats:italic>in vitro<\/jats:italic> and <jats:italic>in vivo<\/jats:italic>, as determined by immunofluorescence assays of 5\u2010ethynyl\u20102'\u2010deoxyuridine (EdU), pH3, Aurora B and CM count, whereas miR\u2010431 inhibition suppresses CM proliferation. Then, we found that miR\u2010431 improved cardiac function post\u2010myocardial infarction. In addition, we identified FBXO32 as a direct target gene of miR\u2010431, with FBXO32 mRNA and protein expression being suppressed by miR\u2010431. FBXO32 inhibited CM proliferation. Overexpression of FBXO32 blocks the enhanced effect of miR\u2010431 on CM proliferation, suggesting that FBXO32 is a functional target of miR\u2010431 during CM proliferation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>In summary, miR\u2010431 promotes CM proliferation by targeting FBXO32, providing a potential molecular target for preventing myocardial injury.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jgm.3656","type":"journal-article","created":{"date-parts":[[2024,1,6]],"date-time":"2024-01-06T12:39:22Z","timestamp":1704544762000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["MiR\u2010431 promotes cardiomyocyte proliferation by targeting FBXO32 expression"],"prefix":"10.1002","volume":"26","author":[{"given":"Mengsha","family":"Li","sequence":"first","affiliation":[{"name":"Panzhou Renze Hospital  Panzhou Guizhou 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