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BRD4 is essential for cardiomyocyte homeostasis. Multiple forms of cardiac stress, including transverse aortic constriction (TAC), myocardial infarction (MI), and genetic defects PLNR9C or LMNA deficiency could be blunted by BD inhibitor JQ1. Recent evidence also suggests that BET protein BRD4 is involved in maintaining mitochondrial homeostasis in cardiomyocyte via a BD-independent mechanism and complete deletion leads to DCM and HF.
