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J Mol Cell Cardiol. 2013 May;58:53-8. doi: 10.1016/j.yjmcc.2013.01.011. Epub 2013 Jan 28.

Pernicious attrition and inter-RyR2 CICR current control in cardiac muscle.

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Rush University Medical Center, Department of Molecular Biophysics & Physiology, Section of Cellular Signaling, 1750 West Harrison Street, Chicago, IL 60612, USA.


In cardiac muscle cells, ryanodine receptor (RyR) mediated Ca(2+) release from the sarcoplasmic reticulum (SR) drives the contractile apparatus. Spontaneous bouts of inter-RyR Ca(2+) induced Ca(2+) release (CICR) generate an elemental unit of SR Ca(2+) release called a spark. Sparks are localized events that terminate soon after they begin. The local control of sparks is not clearly understood. In this article, we review the potential regulatory role that the changing single RyR Ca(2+) current may play. Moreover, we aggregate RyR data into a working scheme of inter-RyR CICR current control of sparks and a potential inter-RyR CICR termination mechanism that we call pernicious attrition.

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