Titin and troponin: Central players in the Frank-Starling mechanism of the heart

Norio Fukuda*, Takako Terui, Iwao Ohtsuki, Shin'ichi Ishiwata, Satoshi Kurihara


    研究成果: Article査読

    40 被引用数 (Scopus)


    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.

    ジャーナルCurrent Cardiology Reviews
    出版ステータスPublished - 2009

    ASJC Scopus subject areas

    • 循環器および心血管医学


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