FTO and myocardial infarction: Overexpression of FTO in the myocardial cells of mice subjected to hypoxia or myocardial infarction reduces fibrosis, promotes angiogenesis, and upregulates the expression of myocardial sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2a (SERCA2a), thereby improving the cardiac systolic function [57].