Abstract
Ca2+ plays a crucial role in connecting membrane excitability with contraction in myocardium. The hallmark features of heart failure are mechanical dysfunction and arrhythmias; defective intracellular Ca homeostasis is a central cause of contractile dysfunction and arrhythmias in failing myocardium. Defective Ca homeostasis in heart failure can result from pathological alteration in the expression and activity of an increasingly understood collection of Ca homeostatic and structural proteins, ion channels, and enzymes. This review focuses on the molecular mechanisms of defective Ca2+ cycling in heart failure and considers how fundamental understanding of these pathways may translate into novel and innovative therapies.
Original language | English (US) |
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Pages (from-to) | 690-708 |
Number of pages | 19 |
Journal | Circulation research |
Volume | 113 |
Issue number | 6 |
DOIs | |
State | Published - 2013 |
Externally published | Yes |
Keywords
- CaMKII
- calcium
- excitation-contraction coupling
- heart failure
- mitochondria
ASJC Scopus subject areas
- Physiology
- Cardiology and Cardiovascular Medicine