Cardiac thin filament regulation and the Frank–Starling mechanism

The heart has an intrinsic ability to increase systolic force in response to a rise in ventricular filling (the Frank–Starling law of the heart). It is widely accepted that the length dependence of myocardial activation underlies the Frank–Starling law of the heart. Recent advances in muscle physiol...

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Bibliographic Details
Published in:The journal of physiological sciences 2014-07, Vol.64 (4), p.221-232
Main Authors: Kobirumaki-Shimozawa, Fuyu, Inoue, Takahiro, Shintani, Seine A., Oyama, Kotaro, Terui, Takako, Minamisawa, Susumu, Ishiwata, Shin’ichi, Fukuda, Norio
Format: Article
Language:English
Subjects:
Animals
Calcium
Cardiac muscle
Cardiac Myosins - metabolism
Connectin - metabolism
Heart - physiology
Humans
Myocardium - metabolism
Review
Sarcomeres - metabolism
Starlings - physiology
Titin
Troponin
Troponin - metabolism
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Summary:The heart has an intrinsic ability to increase systolic force in response to a rise in ventricular filling (the Frank–Starling law of the heart). It is widely accepted that the length dependence of myocardial activation underlies the Frank–Starling law of the heart. Recent advances in muscle physiology have enabled the identification of the factors involved in length-dependent activation, viz., titin (connectin)-based interfilament lattice spacing reduction and thin filament “on–off” regulation, with the former triggering length-dependent activation and the latter determining the number of myosin molecules recruited to thin filaments. Patients with a failing heart have demonstrated reduced exercise tolerance at least in part via depression of the Frank–Starling mechanism. Recent studies revealed that various mutations occur in the thin filament regulatory proteins, such as troponin, in the ventricular muscle of failing hearts, which consequently alter the Frank–Starling mechanism. In this article, we review the molecular mechanisms of length-dependent activation, and the influence of troponin mutations on the phenomenon.
ISSN:1880-6546
1880-6562
DOI:10.1007/s12576-014-0314-y