Key result
Cardiac molecular motors play a dominant role in the intrinsic regulation of ventricular ejection and isovolumic relaxation through cooperative and mechanical feedback mechanisms.
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Design
Review
No immediate clinical implications; extends mechanistic framework for future therapeutic targeting in ventricular dysfunction.
Molecular motors housed in myosins of the thick filament react with thin-filament actins and promote force and shortening in the sarcomeres. However, other actions of these motors sustain sarcomeric activation by cooperative feedback mechanisms in which the actin-myosin interaction promotes thin-filament activation. Mechanical feedback also affects the actin-myosin interaction. We discuss current concepts of how these relatively under-appreciated actions of molecular motors are responsible for modulation of the ejection time and isovolumic relaxation in the beating heart.
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Hinken et al. (2007) reported a review. Cardiac molecular motors play a dominant role in the intrinsic regulation of ventricular ejection and isovolumic relaxation through cooperative and mechanical feedback mechanisms.
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