Abstract
Accumulation of oxidized matrix between the endothelium and cardiac muscle, and endocardial endothelial dysfunction, are the hallmarks of congestive heart failure. The induction of oxidative stress, decrease in endothelial cell density, activation of matrix and disintegrin metalloproteinase, collagenolysis, and repression of cardiac inhibitor of metalloproteinase (CIMP) are associated with deposition of oxidized matrix. Studies that employ CIMP as genetic or proteomic therapeutic agent may improve the heart's response to nitric oxide donors. Identification of major players involved in the control of oxidative and proteolytic stresses that ameliorate matrix deposition by integrin shading will help to develop strategies to prevent congestive heart failure.
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