doi: 10.1161/01.CIR.0000057859.91134.AD
(Circulation. 2003;107:1348.)
© 2003 American Heart Association, Inc.
Editorial |
NO Balance
Regulation of the Cytoskeleton in Congestive Heart Failure by Nitric Oxide
From Molecular Cardiology, Department of Internal Medicine IV, University of Frankfurt, Frankfurt, Germany.
Correspondence to Stefanie Dimmeler, Dept. of Molecular Cardiology, University of Frankfurt, Theodor Stern-Kai 7, 60590 Frankfurt, Germany. E-mail Dimmeler@em.uni-frankfurt.de
Key Words: Editorials • myocytes • nitric oxide • heat failure • cells
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Congestive heart failure is a leading cause of cardiovascular mortality in the United States and Europe.1 Clinically, this syndrome is characterized by water retention and often left ventricular dilatation with poor systolic contractility. Etiologically, congestive heart failure can be of genetic or acquired origin. In 1993, 2 groups independently reported mutations in the cytoskeletal protein dystrophin as the cause of X-linked dilated cardiomyopathy, a rare inheritable disease that leads to enlargement of ventricular dimensions and to congestive heart failure.1 Over the last decade, the pathophysiological relevance of the cardiac myocyte cytoskeleton for the development of congestive heart failure is being increasingly recognized.
See p 1424
For a coordinated contractile function of the heart, the mechanical forces generated within the sarcomeres of individual cardiac myocytes are transmitted to the extracellular matrix.2 For this purpose, cardiac myocytes are equipped with a specialized extrasarcomeric cytoskeleton. The cardiac myocyte cytoskeleton acts as a "scaffold" that provides mechanical stability to transmit the periodic shortening of the sarcomeres to adjacent cardiac myocytes.1 Additionally, the cytoskeleton possesses important signaling properties.3
The critical importance of an intact cytoskeleton for normal cardiac function in humans and rodents is highlighted by genetic defects in the cytoskeletal proteins titin, actin, dystrophin, sarcoglycans, and others, all of which cause dilated cardiomyopathy with congestive heart failure in patients.1,2,4 In the cardiomyopathic hamster, a 
-sarcoglycan deletion has been identified as disease-causing, and targeted deletion of the muscle LIM protein (MLP) in mice results in a dilated cardiomyopathy phenotype.5
MLP is a muscle-specific, LIM-domain only
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