Tectorigenin attenuates cardiac hypertrophy via USP9X/MCL1-mediated mitochondrial stabilization.

ABSTRACT: Pathological cardiac hypertrophy, driven by mitochondrial dysfunction and maladaptive remodeling, remains a therapeutic challenge. This study explores the cardioprotective properties of tectorigenin (Tec) in the context of transverse aortic constriction (TAC)-induced hypertrophy, focusing on mitochondrial homeostasis. In animal models, administration of Tec improved survival rates, reduced cardiac dysfunction, and decreased hypertrophy and fibrosis in TAC mice, while preserving mitochondrial function. In in vitro experiments, Tec was found to inhibit the enlargement of cardiomyocytes and mitochondrial impairment induced by phenylephrine. The underlying mechanism revealed that Tec stabilizes MCL1, a key regulator of mitochondrial integrity, by promoting its deubiquitination through USP9X, t

SUBMITTER: Chen X 

PROVIDER: S-EPMC12446508 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature