Besides, very recently, it has been indicated that the lack of Metrnl is prone to promote cardiac hypertrophy, and the overexpression or treatment of Metrnl can activate the PPARγ coactivator-1α (PGC1-α) and fatty acid oxidation (FAO) pathways of cardiomyocytes to protect heart against cardiac dysfunction in mice (35). Here, PPARGC1A is linked to cardiac hypertrophy.