Regulation of cardiac calcium by mechanotransduction: Role of mitochondria

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 m...

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Bibliographic Details
Published in:Archives of biochemistry and biophysics 2018-12, Vol.659, p.33-41
Main Authors: Kim, Joon-Chul, Son, Min-Jeong, Woo, Sun-Hee
Format: Article
Language:English
Subjects:
Ca2+ signaling
Cardiac myocytes
Mechanical stress
Mitochondria
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Summary: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.
ISSN:0003-9861
1096-0384
DOI:10.1016/j.abb.2018.09.026