Why the study?
Because miRNA-663 regulates TGF-β1, which contributes to myocardial fibrosis, the study aimed to determine whether miRNA-663 participates in myocardial fibrosis via interaction with TGF-β1.
MicroRNA-663 is downregulated in myocardial fibrosis and its overexpression in vitro reduces TGF-β1 and fibrosis markers, suggesting it as a potential therapeutic target.
May support miRNA-663 as a fibrosis target; leaves open clinical translation from in vitro data.
MicroRNA-663 (miRNA-663) regulates the expression of transforming growth factor β1 (TGF-β1), which participates in the pathogenesis of myocardial fibrosis. Therefore, microRNA-663 may also serve a role in myocardial fibrosis. The present study aimed to determine whether miRNA-663 participates in myocardial fibrosis via interaction with TGF-β1. In the present study, the expression of miRNA-663 was significantly downregulated, whereas that of TGF-β1 was significantly upregulated in the endomyocardial biopsies of patients with myocardial fibrosis compared with those in control necropsies. Pearson's correlation analysis revealed that the expression levels of miRNA-663 were negatively correlated with those of TGF-β1 in patients with myocardial fibrosis, but not in the controls. Receiver operating characteristic curve analysis demonstrated that the downregulation of miRNA-663 distinguished patients with myocardial fibrosis from controls. In the AC16 human cardiomyocyte cell line, miRNA-663 overexpression resulted in downregulated TGF-β1 expression, whereas exogenous TGF-β1 treatment exhibited no significant effects on miRNA-663 expression. These results indicate that miRNA-663 may participate in myocardial fibrosis, possibly through interaction with TGF-β1.
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Wu et al. (2019) studied this question.
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