title: Mechanisms of altered Ca²⁺ handling in heart failure.
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 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.
authors.affiliation: Division of Cardiovascular Medicine, Department of Internal Medicine, Cardiovascular Research Center, Carver College of Medicine, University of Iowa, Iowa City, IA, USA.
authors.forename: Min
authors.initials: M
authors.lastname: Luo
authors.forename: Mark E
authors.initials: ME
authors.lastname: Anderson
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D056966:Excitation Contraction Coupling; D006333:Heart Failure / Q000378:metabolism*; D006801:Humans
chemical_list: D002118:Calcium
keywords: CaMKII; calcium; excitation-contraction coupling; heart failure; mitochondria