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However, there is no validated therapy for it. Dysregulation of microRNAs has been confirmed to be involved in cardiac fibrosis development. However, the regulatory network was not well explored. This study was the first to highlight the role and molecular mechanism of miR\u2010409\u20103p in cardiac fibrosis. We found that miR\u2010409\u20103p was consistently increased in three fibrotic models, including heart tissues of postmyocardial infarction (MI) mice and neonatal rat cardiac fibroblasts treated with angiotensin II (Ang II) or transforming growth factor\u2010<jats:italic>\u03b2<\/jats:italic> (TGF\u2010<jats:italic>\u03b2<\/jats:italic>). Furthermore, myocardial infarction surgery\u2010induced cardiac fibrosis and dysfunction were attenuated by systemic delivery of miR\u2010409\u20103p antagomir. Notably, transfection with miR\u2010409\u20103p mimics promoted the proliferation of cardiac fibroblasts and fibroblast\u2010to\u2010myofibroblast differentiation, accompanied by upregulated expression of Col1a1, Col3a1, and <jats:italic>\u03b1<\/jats:italic>\u2010SMA. On the contrary, the miR\u2010409\u20103p inhibitor exhibited the opposite effect. Following this, we verified Gpd1 as a direct target of miR\u2010409\u20103p. Gpd1 siRNA abolished the antifibrotic effect of miR\u2010409\u20103p inhibitor in neonatal rat cardiac fibroblasts, suggesting that miR\u2010409\u20103p promotes cardiac fibrosis at least partially through Gpd1. Moreover, GATA2 was identified as a cardiac fibrosis\u2010associated upstream positive transcription factor of miR\u2010409\u20103p. Finally, these findings suggest that modulating miR\u2010409\u20103p could be a potential therapeutic method for cardiac fibrosis.<\/jats:p>","DOI":"10.1155\/2022\/8922246","type":"journal-article","created":{"date-parts":[[2022,10,12]],"date-time":"2022-10-12T20:50:11Z","timestamp":1665607811000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["miR\u2010409\u20103p Regulated by GATA2 Promotes Cardiac Fibrosis through Targeting 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