Cardiac thin filament regulation.
Myocardial contraction is initiated upon the release of calcium into the cytosol from the sarcoplasmic reticulum following membrane depolarization. The fundamental physiological role of the heart is to pump an amount blood that is determined by the prevailing requirements of the body. The physiological control systems employed to accomplish this task include regulation of heart rate, the amount of calcium release, and the response of the cardiac myofilaments to activator calcium ions. Thin filament activation and relaxation dynamics has emerged as a pivotal regulatory system tuning myofilament function to the beat-to-beat regulation of cardiac output. Maladaptation of thin filament dynamics, in addition to dysfunctional calcium cycling, is now recognized as an important cellular mechanism causing reduced cardiac pump function in a variety of cardiac diseases. Here, we review current knowledge regarding protein-protein interactions involved in the dynamics of thin filament activation and relaxation and the regulation of these processes by protein kinase-mediated phosphorylation.
Kobayashi
Tomoyoshi
T
Department of Physiology & Biophysics, University of Illinois at Chicago, Chicago, IL 60612, USA.
Jin
Lei
L
de Tombe
Pieter P
PP
D008841:Actin Cytoskeleton / Q000378:metabolism / Q000502:physiology* / Q000648:ultrastructure; D000199:Actins / Q000502:physiology; D000818:Animals; D006321:Heart / Q000502:physiology*; D006331:Heart Diseases / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D009206:Myocardium / Q000166:cytology / Q000378:metabolism / Q000648:ultrastructure; D014335:Tropomyosin / Q000502:physiology; D019209:Troponin C / Q000502:physiology; D019210:Troponin I / Q000502:physiology; D020107:Troponin T / Q000502:physiology
D000199:Actins; D014335:Tropomyosin; D019209:Troponin C; D019210:Troponin I; D020107:Troponin T