![]() ![]() Moreover, GATA2 was identified as a cardiac fibrosis-associated upstream positive transcription factor of miR-409-3p. Gpd1 siRNA abolished the antifibrotic effect of miR-409-3p inhibitor in neonatal rat cardiac fibroblasts, suggesting that miR-409-3p promotes cardiac fibrosis at least partially through Gpd1. Following this, we verified Gpd1 as a direct target of miR-409-3p. On the contrary, the miR-409-3p inhibitor exhibited the opposite effect. Notably, transfection with miR-409-3p mimics promoted the proliferation of cardiac fibroblasts and fibroblast-to-myofibroblast differentiation, accompanied by upregulated expression of Col1a1, Col3a1, and α-SMA. Furthermore, myocardial infarction surgery-induced cardiac fibrosis and dysfunction were attenuated by systemic delivery of miR-409-3p antagomir. We found that miR-409-3p 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- β (TGF- β). This study was the first to highlight the role and molecular mechanism of miR-409-3p in cardiac fibrosis. However, the regulatory network was not well explored. Dysregulation of microRNAs has been confirmed to be involved in cardiac fibrosis development. However, there is no validated therapy for it. Cardiac fibrosis is a hallmark of numerous chronic cardiovascular diseases that leads to heart failure. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |