MLKL and cardiac hypertrophy: Our results showed that (1) RIP3 protein expression was significantly increased in the pressure- and drug-treated models of myocardial hypertrophy; (2) loss function of RIP3 by shRNAs in rats reduced myocardial hypertrophy, and oe-RIP3 rats increased myocardial hypertrophy; (3) RIP3 interacts with MLKL to localize intracellular membrane-mediated calcium influx, thus promoting cardiomyocyte hypertrophy; and (4) blockage of calcium influx reverses RIP3-mediated exacerbation of cardiac remodeling.