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Updated: Aug 19, 2026

Analysis of Cardiac Contractile Dysfunction and Ca2+ Transients in Rodent Myocytes
Published on: May 25, 2022
Cardiac mechanotransduction and implications for heart disease
Ralph Knöll1, Masahiko Hoshijima, Kenneth Chien
1Institute of Molecular Medicine, University of California at San Diego, 9500 Gilman Drive Mail Code 0641, La Jolla, CA 92093-0641, USA. rknoell@ucsd.edu
Abstract:
Mechanotransduction, the conversion of a mechanical stimulus into a cellular response, plays a fundamental role in cell volume regulation, fertilization, gravitaxis, proprioception, and the senses of hearing, touch, and balance. Mechanotransduction also fills important functions in the myocardium, where each cycle of contraction and relaxation leads to dynamic deformations. Since the initial observation of stretch induced muscle growth, our understanding of this complex field has been steadily growing, but remains incomplete. For example, the mechanism by which myocytes sense mechanical forces is still unknown. It is also unknown which mechanism converts such a stimulus into an electrochemical signal, and how this information is transferred to the nucleus. Is there a subpopulation of mechanosensing myocytes or mechanosensing cells in the myocardium? The following article offers an overview of the fundamental processes of mechanical stretch sensing in myocytes and recent advances in our understanding of this increasingly important field. Special emphasis is placed on the unique cardiac cytoskeletal structure and related Z-disc proteins.
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