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Current Cardiology Reviews
ISSN (Print): 1573-403X
ISSN (Online): 1875-6557
VOLUME: 5
ISSUE: 2
DOI: 10.2174/157340309788166714      Price:  $58









Titin and Troponin: Central Players in the Frank-Starling Mechanism of the Heart

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Author(s): Norio Fukuda, Takako Terui, Iwao Ohtsuki, Shin'ichi Ishiwata and Satoshi Kurihara
Pages 119-124 (6)
Abstract:
The basis of the Frank-Starling mechanism of the heart is the intrinsic ability of cardiac muscle to produce greater active force in response to stretch, a phenomenon known as length-dependent activation. A feedback mechanism transmitted from cross-bridge formation to troponin C to enhance Ca2+ binding has long been proposed to account for length-dependent activation. However, recent advances in muscle physiology research technologies have enabled the identification of other factors involved in length-dependent activation. The striated muscle sarcomere contains a third filament system composed of the giant elastic protein titin, which is responsible for most passive stiffness in the physiological sarcomere length range. Recent studies have revealed a significant coupling of active and passive forces in cardiac muscle, where titin-based passive force promotes cross-bridge recruitment, resulting in greater active force production in response to stretch. More currently, the focus has been placed on the troponin-based “on-off” switching of the thin filament state in the regulation of length-dependent activation. In this review, we discuss how myocardial lengthdependent activation is coordinately regulated by sarcomere proteins.
Keywords:
Calcium, cardiac muscle, connectin
Affiliation:
Department of Cell Physiology, The Jikei University School of Medicine, 3-25-8 Nishishinbashi, Minato-ku, Tokyo 105-8461, Japan.