ATP2B1 and myocardial infarction: As reported in a previous study, ATP2B1-AS1 was highly expressed in mice with myocardial infarction, while silencing of mouse ATP2B1-AS1 reduced cardiomyocyte apoptosis and inhibited the expression of inflammatory cytokines, as well as promoted the cardiomyocyte viability (Song et al., 2020).