Regulation of cardiac calcium by mechanotransduction: Role of mitochondria

Abstract

Myocardium is subjected to a variety of forces with each contraction, such as stretch, afterload, and shear stress, and adapts to those mechanical stimuli. These mechanical stimuli increase in heart failure, valvular heart disease and hypertension that are clinically associated with arrhythmia and myocyte remodeling. To understand cellular and molecular basis of mechanical stress-mediated cardiac dysfunction and remodeling, several experimental approaches have been successfully used in single cardiac myocytes. In this review, we will briefly summarize the current knowledge about the responses of cardiac myocytes to mechanical stimuli and underlying mechanisms in the context of Ca²⁺ signaling, with focusing on the role of mitochondria in these mechanotransductions. Recent evidence suggests that mechanotransduction, associated with mitochondrial metabolism, significantly alters Ca²⁺ signaling and ionic homeostasis in cardiac myocytes under shear stress or prolonged stretch, and that it may play a key role in the pathogenesis of heart failure.

Keywords: Ca(2+) signaling; Cardiac myocytes; Mechanical stress; Mitochondria.