de Tombe Pieter P
Department of Physiology and Biophysics, and Cardiovascular Science Program, College of Medicine, University of Illinois, 900 S. Ashland Ave, Chicago, IL 60607-7171, USA.
J Biomech. 2003 May;36(5):721-30. doi: 10.1016/s0021-9290(02)00450-5.
The mechanical properties of the cardiac myofilament are an important determinant of pump function of the heart. This report is focused on the regulation of myofilament function in cardiac muscle. Calcium ions form the trigger that induces activation of the thin filament which, in turn, allows for cross-bridge formation, ATP hydrolysis, and force development. The structure and protein-protein interactions of the cardiac sarcomere that are responsible for these processes will be reviewed. The molecular mechanism that underlies myofilament activation is incompletely understood. Recent experimental approaches have been employed to unravel the mechanism and regulation of myofilament mechanics and energetics by activator calcium and sarcomere length, as well as contractile protein phosphorylation mediated by protein kinase A. Central to these studies is the question whether such factors impact on muscle function simply by altering thin filament activation state, or whether modulation of cross-bridge cycling also plays a part in the responses of muscle to these stimuli.
心肌肌丝的力学特性是心脏泵功能的重要决定因素。本报告聚焦于心肌中肌丝功能的调节。钙离子形成触发因素，诱导细肌丝激活，进而允许形成横桥、ATP水解和产生力量。将对负责这些过程的心脏肌节的结构和蛋白质-蛋白质相互作用进行综述。肌丝激活的分子机制尚未完全明确。最近已采用实验方法来阐明激活剂钙和肌节长度以及蛋白激酶A介导的收缩蛋白磷酸化对肌丝力学和能量学的作用机制及调节。这些研究的核心问题是，这些因素是仅仅通过改变细肌丝激活状态来影响肌肉功能，还是横桥循环的调节在肌肉对这些刺激的反应中也起作用。
