In cardiac regeneration models, CPT1 inhibition reverses metabolic reprogramming and reduces PARP1‐mediated DUSP1 PARylation, leading to decreased p38 mitogen‐activated protein kinase (MAPK) phosphorylation and activation of adult cardiomyocyte proliferation post‐myocardial infarction [184]. Here, PARP1 is linked to myocardial infarction.