Zinc controls RyR2 activity during excitation-contraction coupling
Abstract
Cardiac excitation-contraction (EC) coupling is a process which governs contractility of the heart through the controlled release of Ca2+ from the sarcoplasmic reticulum (SR). The type-2 ryanodine receptor (RyR2) is the route through which Ca2+ is released from the SR providing the necessary driving force for cellular contraction. In heart failure, RyR2-channels become abnormally active, or ‘leaky’, and are unable to remain closed during diastole resulting in unwanted irregular contractile and electrical activity1. Defective Zn2+ handling has been shown to contribute to the cellular pathology of certain cardiomyopathies which give rise to impaired contractility including heart failure 2. This is likely a consequence of altered EC coupling as a result of modified RyR2 function. How zinc impacts upon the contractile force and the release of calcium from intracellular stores in heart is not fully understood.
Citation
Stewart , A J & Pitt , S J 2015 , ' Zinc controls RyR2 activity during excitation-contraction coupling ' , Channels , vol. 9 , no. 5 , pp. 223-225 . https://doi.org/10.1080/19336950.2015.1075784
Publication
Channels
Status
Peer reviewed
ISSN
1933-6950Type
Journal article
Rights
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.
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