Year: 2013
Type: review
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.
Source: Circulation Research
Authors: Min Luo, Mark E. Anderson
Institution: University of Iowa
Language: English
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W2118103758