PRKN and myocardial infarction: In our study, it was found that (i) RIPK3 could be activated after MI and would facilitate the development of post-MI cardiac remodelling; (ii) genetic ablation of Ripk3 alleviated cardiac remodelling and promoted the cardiac function and survival of MI mice; (iii) Ripk3 upregulation in cardiomyocytes inhibited AMPK phosphorylation, which reduced Parkin activation, thereby inhibiting mitophagy; and (iv) inactivation of mitophagy promoted opening of the mPTP, leading to cardiomyocyte necroptosis.