FOXO3a-dependent PARKIN negatively regulates cardiac hypertrophy by restoring mitophagy.

ABSTRACT:

Background

Sustained cardiac hypertrophy often develops maladaptive myocardial remodeling, and eventually progresses to heart failure and sudden death. Therefore, maladaptive hypertrophy is considered as a critical therapeutic target for many heart diseases. Mitophagy, a crucial mechanism in mitochondria quality control and cellular homeostasis, has been implicated in diverse cardiac disorders such as myocardial infarction, diabetic cardiomyopathy, cardiac hypertrophy and heart failure. However, what role mitophagy plays in heart diseases remains an enigma. PARKIN functions as an E3 ubiquitin protein ligase and mediates mitophagy cascades. It is still unclear whether PARKIN participates in the regulation of cardiac hypertrophy.

Results

PARKIN was downregulated in cardiomyocy

SUBMITTER: Sun T 

PROVIDER: S-EPMC9764573 | biostudies-literature | 2022 Dec

REPOSITORIES: biostudies-literature