New Support For A Controversial Mechanism Underlying An Irregular Heart Beat
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The most common form of human heart beat irregularity (atrial fibrillation) can be fatal if left untreated. It has been suggested that it is caused, in part, by calcium leaking from a cellular store in heart cells, potentially through the RyR2 channel, although this mechanism remains controversial. However, a team of researchers at Baylor College of Medicine, Houston, and Dresden University of Technology, Germany, has provided support for this hypothesis by showing that the protein CaMKII can enhance RyR2-mediated calcium leak, promoting atrial fibrillation in mice.
The team, led by Xander Wehrens and Dobromir Dobrev, studied mice engineered to express a mutant form of RyR2 associated with calcium leak. Although these mice did not spontaneously develop atrial fibrillation, they were more likely to develop atrial fibrillation than normal mice if their heart rate was forced up. This was related to the functional interaction of CaMKII with RyR2, and blocking CaMKII function in these mice prevented them from developing atrial fibrillation when their heart rate was forced up. As a functional link between CaMKII and RyR2 was observed in heart biopsies from patients with chronic atrial fibrillation, the authors suggest that enhanced CaMKII function might increase calcium leakage via RyR2 and initiate clinical atrial fibrillation.
TITLE: Calmodulin kinase II - mediated sarcoplasmic reticulum Ca2+ leak promotes atrial fibrillation in mice
Xander H.T. Wehrens
Baylor College of Medicine, Houston, Texas, USA.
Dresden University of Technology, Dresden, Germany.
View the PDF of this article at: https://www.the-jci.org/article.php?id=37059
Journal of Clinical Investigation
JCI online early table of contents: June 15, 2009
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