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Review
. 2009 Jul 1;587(Pt 13):3091-4.
doi: 10.1113/jphysiol.2009.172049.

Cardiac calsequestrin: quest inside the SR

Sandor Györke  1 , Sarah C W Stevens, Dmitry Terentyev
Affiliations
Review

Cardiac calsequestrin: quest inside the SR

Sandor Györke et al. J Physiol. .
No abstract available

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Figures

Figure 1
Figure 1. Ca2+ handling in myocytes from normal hearts and hearts lacking CASQ2
In a normal myocyte, Ca2+ release from the SR evoked by Ca2+ entry through voltage-dependent Ca2+ channels (LCCs) results in a decline of [Ca2+] in the SR. As [Ca2+]SR declines, Ca2+ dissociates from CASQ2 and the Ca2+-free CASQ2 monomers bind to and inhibit RyR2s causing Ca2+ release to terminate at a certain threshold [Ca2+]SR. The SR Ca2+ store stays refractory for some time after luminal Ca2+ is recovered by the SERCA2 pump and Ca2+-bound CASQ2 dissociates from TRD. This prevents spontaneous Ca2+ release during diastole. In myocytes lacking CASQ2, reduced SR Ca2+ binding capacity is compensated by increased SR Ca2+ volume. In the absence of the inhibitory influence of CASQ2 increased leak through the RyR2 results in reduced basal [Ca2+]SR. In addition, the RyR2s lack the capacity to deactivate until nearly complete depletion stops CICR and store refractoriness is substantially shortened predisposing the SR to premature SR Ca2+ release. Extrasystolic elevation of [Ca2+]c evokes pro-arrhythmic delayed afterdepolarizations (DADs) by stimulating the Na+/Ca2+ exchanger (NCX).
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