In summary, the authors concluded that in animal model, overexpression of irisin alleviated myocardial hypertrophy induced by pressure overload reducing cardiomyocytes apoptosis and that irisin protection against pressure overload-induced cardiac hypertrophy is due to induction of protective autophagy and autophagy flux via activating AMPK-ULK1 signaling [166]. Here, ULK1 is linked to cardiac hypertrophy.