USP10 protects against pressure overload-induced mitochondrial morphofunctional defects and pathological cardiac hypertrophy through stabilizing cytoplasmic Mfn2.

ABSTRACT: Increasing evidence has implicated the important role of mitochondrial morphofunctional defects in pathological myocardial hypertrophy and heart failure. Deubiquitinating enzymes (DUBs) are involved in protein stability maintenance and regulate multiple cellular processes, while it remains largely unclear whether DUBs participate in the maintenance of mitochondrial morphofunction. The aim of this study was to investigate the possible link between DUBs and abnormal mitochondrial morphofunction in pressure overload-induced pathological cardiac hypertrophy and explore the underlying molecular mechanism. RNA sequencing results showed that ubiquitin-mediated proteolysis was markedly enriched in pressure overload-induced hypertrophied and failing myocardium, and USP10 was identified as the most

SUBMITTER: Li R 

PROVIDER: S-EPMC12274942 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature