Subsequent in vivo studies revealed that pirfenidone attenuated Ang II-induced myofibroblast differentiation and fibrosis by decreasing PARP9 expression triggered by Ang II.354 Consistently, PARP inhibition prevented the cardiac hypertrophy and contractile dysfunction in pressure overload-induced heart failure.355 Also, PARP inhibition could offer a promising new therapeutic approach to prevent postinfarction myocardial remodeling.356 However, the role of PARP9 in detecting cytoplasmic dsRNA and facilitating type I interferon production in relation to CVDs remains poorly understood. This evidence concerns the gene PARP9 and cardiac hypertrophy.