Li et al. studied the effects of irisin on myocardial hypertrophy in different models including angiotensin II (Ang II) or phenylephrine (PE) treated cardiomyocyte or mouse aortic transverse contraction (TAC) models and demonstrated that irisin regulated autophagy via mTOR (mechanistic target of rapamycin) independent activation of the AMPK-ULK1 pathway, thereby relieving myocardial hypertrophy [69,85]. This evidence concerns the gene ULK1 and cardiac hypertrophy.