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This editorial discusses the debate regarding the mechanisms of altered calcium handling in heart failure, highlighting the roles of SERCA and the ryanodine receptor.
This editorial discusses the debate surrounding the mechanisms of altered calcium handling in heart failure, specifically focusing on the sarcoplasmic reticulum Ca2+-ATPase and the ryanodine receptor.
I n heart failure, the amplitude and rate of decay of both contraction and the underlying systolic Ca 2ϩ transient are reduced.A current debate concerns the mechanism of these alterations of calcium handling.One theory invokes decreased activity of the sarcoplasmic reticulum (SR) Ca 2ϩ -ATPase (SERCA) 1 while another focuses on alterations in the SR Ca 2ϩ release channel (ryanodine receptor, RyR). 2 A significant contribution to this debate is made by Jiang et al 3 in this issue of Circulation Research.
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Eisner et al. (2002) conducted an editorial in Heart failure. This editorial discusses the debate regarding the mechanisms of altered calcium handling in heart failure, highlighting the roles of SERCA and the ryanodine receptor.
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