Abstract

Congestive heart failure is the leading cause of death in the Western world. Abnormal intracellular calcium (Ca²⁺) handling is central to the pathogenesis of heart failure because it contributes to a decrease in ventricular contractile function. Chronic hyperactivity of the sympathetic nervous system causes increased phosphorylation of the ryanodine receptor intracellular Ca²⁺-release channel, a key Ca²⁺-handling protein in the heart, by protein kinase A. Alteration of the structure and function of ryanodine receptors contributes to defective intracellular Ca²⁺ handling and an increased propensity for cardiac arrhythmias in failing hearts. Novel therapeutic strategies are now being evaluated to specifically correct defective Ca²⁺-handling in heart failure.

Author affiliations

1. Department of Physiology and Cellular Biophysics, Center for Molecular Cardiology, Department of Medicine, Columbia University College of Physicians and Surgeons, 630W 168th Street, P&S 9-401, New York, New York 10032, USA.

Correspondence to: Andrew R. Marks¹ Email: arm42@columbia.edu

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