Targeting Cardiac Hypertrophy Through a Nuclear Co-Repressor

The study by Li et al. demonstrated that the nuclear receptor co-repressor 1 (NCoR1) played a crucial role in inhibiting pathological cardiac hypertrophy and dysfunction by stabilizing the complex between myocyte enhancer factor 2 (MEF2) and class II histone deacetylases (HDACs). Using mutant mice with cardiomyocyte-specific knock-out of NCoR1, the researchers observed increased myocardial hypertrophy and impaired cardiac function, which was mediated by MEF2. Overexpression of the receptor interaction domains (RID) of NCoR1 was sufficient to inhibit hypertrophy and cardiac dysfunction in mice, suggesting that targeting the NCoR1/MEF2/class II HDACs axis could be a potential therapeutic strategy for treating pathological cardiac hypertrophy.