Regulation of sarcoplasmic reticulum Ca2+-ATPase and phospholamban in the failing and nonfailing heart
Open Access
- 1 January 2000
- journal article
- editorial
- Published by Oxford University Press (OUP) in Cardiovascular Research
- Vol. 45 (1) , 245-252
- https://doi.org/10.1016/s0008-6363(99)00338-7
Abstract
The mammalian organism responds to chronic pressure and volume overload of the heart with a plethora of adaptive changes that consist of resetting of the neurohumoral homeostasis on a more general level and of structural remodeling and functional alterations on the cellular level. These latter changes include electrophysiological properties as exemplified by prolongation in action potential duration and rhythm disturbances considered responsible for sudden cardiac death as well as depression in contractile function of individual myocytes. Since calcium ions (Ca2+) play a pivotal role in cardiac excitation–contraction coupling, contractile dysfunction has been interpreted as a defect in Ca2+-handling proteins of the sarcoplasmic reticulum (SR) at the subcellular level.Keywords
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