Journal
CIRCULATION RESEARCH
Volume 112, Issue 2, Pages 355-366Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCRESAHA.112.268672
Keywords
Ca sensitization; Ca signaling; cardiac hypertrophy; ventricular myocytes; Z-disk
Funding
- National Institutes of Health [RO1 HL 064035, RO1 HL 022231, PO1 062426, T32 007692]
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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. (Circ Res. 2013;112:355-366.)
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