Recent studies report exogenous irisin administration alleviates pressure overload-induced cardiac hypertrophy by activating ULK1 autophagy pathway, whereas endogenous irisin knockout disrupts mitochondrial homeostasis and significantly decreases cardiac differentiation in mouse embryonic stem cells (Li et al., 2018; Nazem et al., 2018). This evidence concerns the gene FNDC5 and cardiac hypertrophy.