Abstract
The Na+/Ca2+ exchanger (NCX) is the main Ca2+ extrusion mechanism of the cardiac myocyte and thus is crucial for maintaining Ca2+ homeostasis. It is involved in the regulation of several parameters of cardiac excitation contraction coupling, such as cytosolic Ca2+ concentration, repolarization and contractility. Increased NCX activity has been identified as a mechanism promoting heart failure, cardiac ischemia and arrhythmia. Transgenic mice as well as pharmacological interventions have been used to support the idea of using NCX inhibition as a future pharmacological strategy to treat cardiovascular disease.
Keywords: Na+/Ca2+ exchanger, arrhythmia, ischemia, heart failure, transgenic mice, Ca2+ handling, NCX, genetic knockout, hypertension, cardiovascular disease
Current Drug Targets
Title: Triple Threat: The Na+/Ca2+ Exchanger in the Pathophysiology of Cardiac Arrhythmia, Ischemia and Heart Failure
Volume: 12 Issue: 5
Author(s): Christian Pott, Lars Eckardt and Joshua I. Goldhaber
Affiliation:
Keywords: Na+/Ca2+ exchanger, arrhythmia, ischemia, heart failure, transgenic mice, Ca2+ handling, NCX, genetic knockout, hypertension, cardiovascular disease
Abstract: The Na+/Ca2+ exchanger (NCX) is the main Ca2+ extrusion mechanism of the cardiac myocyte and thus is crucial for maintaining Ca2+ homeostasis. It is involved in the regulation of several parameters of cardiac excitation contraction coupling, such as cytosolic Ca2+ concentration, repolarization and contractility. Increased NCX activity has been identified as a mechanism promoting heart failure, cardiac ischemia and arrhythmia. Transgenic mice as well as pharmacological interventions have been used to support the idea of using NCX inhibition as a future pharmacological strategy to treat cardiovascular disease.
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Cite this article as:
Pott Christian, Eckardt Lars and I. Goldhaber Joshua, Triple Threat: The Na+/Ca2+ Exchanger in the Pathophysiology of Cardiac Arrhythmia, Ischemia and Heart Failure, Current Drug Targets 2011; 12 (5) . https://dx.doi.org/10.2174/138945011795378559
DOI https://dx.doi.org/10.2174/138945011795378559 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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