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Research points to way to improve heart treatment
Date:3/10/2010

events that result in arrhythmia and cell death," said Anderson, who also is a member of the University of Iowa Heart and Vascular Center and holds the Francois Abboud Chair in Internal Medicine.

Using rabbit heart cells, which behave much like human heart cells, the team showed that if CaM kinase is prevented from interacting with a protein that regulates calcium channels, negative effects, including cell death, do not occur. Specifically, they showed it was possible to either block the specific site on the protein where CaM kinase binds or block the ability of CaM kinase to perform phosphorylation on the protein.

In both cases, blocking the action of CaM kinase prevented too much calcium activity, which can be harmful.

"CaM kinase is needed to maintain calcium channel function, which allows the heart to contract. But too much CaM kinase, and consequently too much calcium entry into heart cells, causes electrical instability and other downstream molecular problems that can lead to cell overload and cell death, which causes heart failure," Anderson said.

Anderson said a next step is to try to develop drugs to prevent the unwanted CaM kinase effects.


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Contact: Becky Soglin
becky-soglin@uiowa.edu
319-356-7127
University of Iowa
Source:Eurekalert

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