Cardiac-Specific Deletion of Voltage Dependent Anion Channel 2 Leads to Dilated Cardiomyopathy by Altering Calcium Homeostasis

Scientists generated a cardiac ventricular myocyte-specific developmental deletion of Vdac2 in mice and indicated that loss of VDAC2 in the myocardium caused severe impairment in excitation-contraction coupling by altering both intracellular and mitochondrial calcium signaling.