Department of Physiology and Biophysics and Center for Cardiovascular Research, University of Illinois at Chicago, College of Medicine, Chicago, IL 60612, USA.
Circ Res. 2013 Jan 18;112(2):355-66. doi: 10.1161/CIRCRESAHA.112.268672.
We focus here on the modulation of thin filament activity by cardiac troponin I phosphorylation as an integral and adaptive mechanism in cardiac homeostasis and as a mechanism vulnerable to maladaptive response to stress. We discuss a current concept of cardiac troponin I function in the A-band region of the sarcomere and potential signaling to cardiac troponin I in a network involving the ends of the thin filaments at the Z-disk and the M-band regions. The cardiac sarcomere represents a remarkable set of interacting proteins that functions not only as a molecular machine generating the heartbeat but also as a hub of signaling. We review how phosphorylation signaling to cardiac troponin I is integrated, with parallel signals controlling excitation-contraction coupling, hypertrophy, and metabolism.
我们在这里重点关注心肌肌钙蛋白 I 磷酸化对细肌丝活性的调节，这是心脏内稳态的一个组成和适应性机制，也是对压力的适应不良反应的脆弱机制。我们讨论了心肌肌钙蛋白 I 在肌节 A 带区域的功能的一个当前概念，以及在涉及 Z 盘和 M 带区域的细肌丝末端的网络中对心肌肌钙蛋白 I 的潜在信号转导。心脏肌节代表了一组相互作用的蛋白质，不仅作为产生心跳的分子机器，而且作为信号转导的中心发挥作用。我们回顾了心肌肌钙蛋白 I 的磷酸化信号转导是如何整合的，以及平行信号如何控制兴奋-收缩偶联、肥大和代谢。
