Calcium Ca2+ regulation is a key component of numerous cellular functions. In cardiomyocytes, Ca2+ regulates excitation-contraction coupling and influences signaling cascades involved in cell metabolism and cell survival. Prolonged dysregulation of mitochondrial Ca2+ leads to dysfunctional cardiomyocytes, apoptosis and ultimately heart failure. VEGF promotes cardiomyocyte contractility by increasing calcium transients to control the strength of the heartbeat. Here, we describe a method to measure mitochondrial Ca2+ fluxes in human ventricular cardiomocytes after inducing stretch-mediated hypertrophy in vitro.
Keywords: AC16; Calcium; Cardiomyocyte; Cyclic stretch; Hypertrophy; Mechanotransduction.
© 2022. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.