Targeting Cardiac Hypertrophy Through a Nuclear Co-Repressor

Li et al. demonstrated that the nuclear receptor co-repressor 1 (NCoR1) played a crucial role in inhibiting pathological cardiac hypertrophy by stabilizing the interaction between myocyte enhancer factor 2 (MEF2) and class II histone deacetylases (HDACs). In their study, mice with cardiomyocyte-specific knock-out of NCoR1 developed myocardial hypertrophy and impaired cardiac function, highlighting the importance of NCoR1 in preventing heart overgrowth. The findings suggested that targeting the NCoR1/MEF2/class II HDACs axis could be a potential therapeutic strategy for treating heart failure. However, the regulation of NCoR1 itself and its broader implications in cardiac function required further investigation.