Cardiac-specific overexpression of PRMT5 exacerbates pressure overload-induced hypertrophy and heart failure.

ABSTRACT:

Background

Various epigenetic modifiers are involved in the regulation of gene expression during pathological cardiac hypertrophy-a critical event in the development of heart failure. Our previous research has demonstrated that protein arginine methyltransferase 5 (PRMT5) in cardiac fibroblasts is a crucial epigenetic writer implicated in pathological cardiac fibrosis. Moreover, treatment with a PRMT5 inhibitor also suppressed cardiac hypertrophy in mice after transverse aortic constriction (TAC) surgery. However, as the functional role of PRMT5 in cardiomyocytes remains to be fully elucidated in pathological cardiac hypertrophy and systolic dysfunction, this study aimed to clarify the gain-of-function of PRMT5 in cardiomyocytes.

Methods

Cardiac-specific PRMT5 transgenic (PR

SUBMITTER: Katanasaka Y 

PROVIDER: S-EPMC12229037 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature