Journal
CIRCULATION RESEARCH
Volume 113, Issue 6, Pages 690-708Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCRESAHA.113.301651
Keywords
calcium; CaMKII; excitation-contraction coupling; heart failure; mitochondria
Funding
- University of Iowa Cardiovascular Center Interdisciplinary Research Fellowship Training Grant from National Institutes of Health
- National Institutes of Health [R01HL70250, R01HL079031, R01HL113001, R01HL096652]
- Fondation Leducq as part of the Alliance for CaMKII Signaling in Heart [08CVD01]
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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 Ca2+ homeostasis is a central cause of contractile dysfunction and arrhythmias in failing myocardium. Defective Ca2+ homeostasis in heart failure can result from pathological alteration in the expression and activity of an increasingly understood collection of Ca2+ 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.
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