Other findings have shown that P53 signaling plays a fundamental role in the development of pathological remodeling and heart failure after MI [132], while Bari et al. showed that miR-125b enriched MSCs- exosomes could suppress the expression of the pro-apoptotic genes p53 and Bcl2-antagonist/killer 1 (BAK1) in cardiomyocytes (CMC) in vitro, and also ameliorate ischemic damages in the injured heart and induce noticeable CMC activities post-MI after systemic injection into MI mice models [133]. Here, BAK1 is linked to heart failure.