Background: Myocardial fibrosis after myocardial infarction (MI) has been considered a core factor
in the deterioration of cardiac function. Previous studies have shown that miRNA plays an important role in
various pathophysiological processes of the heart. However, the role of miRNA in myocardial fibrosis regulation
after MI remains unclear. In the present study, we documented that miR-218-5p was significantly decreased
in myocardial fibroblasts after MI.
Methods: The miRNA expression profiles of MI were downloaded from GEO Datasets. The expression of a
fibrosis-related gene in vivo and in vitro was analyzed by RT-PCR, western blotting, and immunohistochemical
Results: Total 7 up- and 9 downregulated common miRNAs were found in the two profiles. Among these
common genes, miR-218-5p was downregulated in the MI mice. MiR-218-5p mediated the myocardial fibrosis
in vivo and in vitro. Mechanistically, we found that GJA1 (CX43) may be the target of miR218-5p, and overexpressed
CX43 can partly block the function of miR-218-5p in fibrosis inhibition.
Conclusion: Our results suggested that miR-218-5p plays an important role in myocardial fibrosis after MI by
targeting CX43. Thus, miR-218-5p promises to be a potential diagnosis and treatment of myocardial fibrosis