Integration of troponin I phosphorylation with cardiac regulatory networks

Circ Res. 2013 Jan 18;112(2):355-66. doi: 10.1161/CIRCRESAHA.112.268672.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Cardiomegaly / metabolism
  • Cardiomegaly / physiopathology
  • Cardiovascular Physiological Phenomena*
  • Humans
  • Myocytes, Cardiac / metabolism*
  • Myocytes, Cardiac / pathology
  • Myocytes, Cardiac / physiology
  • Phosphorylation / physiology
  • Troponin I / metabolism*
  • Troponin I / physiology

Substances

  • Troponin I