The roles and mechanisms of epigenetic regulation in pathological myocardial remodeling

Abstract

Pathological myocardial remodeling was still one of the leading causes of death worldwide with an unmet therapeutic need. A growing number of researchers have addressed the role of epigenome changes in cardiovascular diseases, paving the way for the clinical application of novel cardiovascular-related epigenetic targets in the future. In this review, we summarized the emerged advances of epigenetic regulation, including DNA methylation, Histone posttranslational modification, Adenosine disodium triphosphate (ATP)-dependent chromatin remodeling, Non-coding RNA, and RNA modification, in pathological myocardial remodeling. Also, we provided an overview of the mechanisms that potentially involve the participation of these epigenetic regulation.

Epigenetic Regulation of Fibroblasts and Crosstalk between Cardiomyocytes and Non-Myocyte Cells in Cardiac Fibrosis

“…Regarding MBPs, current research has found that methyl-CpG binding protein 2 (MeCP2), as a protein containing MBD, participates in the regulation of cardiac fibroblast proliferation and fibrosis via its ability to bind methylated DNA. In the transverse aortic constriction (TAC) mouse model, inhibiting MeCP2 activates fibroblasts and aggravates cardiac fibrosis [ 50 ], while the overexpression of MeCP2 alone shows lower levels of fibrosis and good cardiac repair [ 51 ]. Tao et al’s research on the mechanism of MeCP2 action showed that the use of MeCP2 inhibitors to treat cardiac fibroblasts can increase the expression of dual-specificity phosphatase 5 (DUSP5), and DUSP5 negatively regulates the ERK signaling pathway, thus promoting myocardial fibrosis [ 39 ].…”