Socking It to Cardiac Hypertrophy STIM1-Mediated Ca Entry in the Cardiomyocyte

In the heart, increases in contractile load provoked by hypertension or valvular disease promote increases in cardiac mass through the hypertrophy of cardiomyocytes. Injury or death to cardiomyocytes in a portion of the heart places a greater load on cells within uninjured areas and stimulates cellular hypertrophy. Similarly, in familial forms of hypertrophic cardiomyopathy, defects in genes encoding proteins of the sarcomere promote growth in the absence of a stimulus. Hypertrophic hearts are susceptible to abnormalities of cardiac rhythm and have impaired relaxation (diastolic dysfunction), although contractile performance can be preserved. However, when hypertrophic stimuli are unrelieved, the remodeling phenomenon progresses and increasing numbers of cardiomyocytes are replaced with fibrotic scar, which leads to decreased systolic function and circulatory failure.