![]() | Only 14 pages are availabe for public view |
Abstract Pediatric dilated cardiomyopathy (DCM) is the most common and most aggressive form of cardiomyopathy in children. It is a multifactorial heart disease in which there is enlargement and systolic dysfunction of one or both ventricles. The exhaustion of compensatory mechanisms leads to symptoms and signs of congestive heart failure, where death or transplantation within one year of the initial diagnosis is a common outcome. Left ventricular (LV) dilatation and myocardial remodeling are hallmarks of heart failure in idiopathic DCM. Interstitial collagen is essential for LV integrity and function while degradation of collagen by collagenases, especially matrix-metalloproteinases (MMPs), is suggested to contribute to ventricular dilatation. Matrix metalloproteinases (MMPs) are a family of zinc and calcium-dependent proteolytic enzymes that are regulated by inflammatory signals to mediate changes in extracellular matrix. MMP- 3, or stromelysin-1, is an important constituent of the MMP family because of its ability to degrade a wide range of extracellular matrix components. |