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Zinc controls RyR2 activity during excitation-contraction coupling

Research output: Contribution to journalArticlepeer-review

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.

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Details

Original languageEnglish
Pages (from-to)223-225
JournalChannels
Volume9
Issue number5
Early online date28 Jul 2015
DOIs
Publication statusPublished - Sep 2015

    Research areas

  • Ryanodine receptor, Excitation-contraction coupling, Ca2+-release, Zn2+-signalling, Cardiomyocyte

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ID: 204377371

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