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The Mechanisms of the Frank-Starling Law and Familial Cardiomyopathy are Different. The Function of Myosin Binding Protein-C is Retained on Myocyte Length Increase and Force Generated is Kinase controlled
: Received: 4 October 2019 / Approved: 7 October 2019 / Online: 7 October 2019 (12:15:26 CEST)
A peer-reviewed article of this Preprint also exists.
Journal reference: J. Integr. Cardiol. 2019, 5, 1-3
I have recently reiterated that the cross-bridge is a calcium ATPase that is inhibited by magnesium and this arises because in normal hearts Myosin binding Protein-C prevents the use of MgATP as rate limiting substrate ensuring that Ca2+ replaces Mg2+ in the excitation pathway. Here I revisit the studies on [Ca2+] dependency of ATPase and tension under diastolic stretch with a different conclusion on Hill coefficients. This reveals the underlying mechanisms of the Frank-Starling Law and Hypertrophic myopathy are not the same, the former being kinase controlled.
Frank-Starling; myopathy; Myosin Binding Protein-C; Kinase mechanism
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