Integration of concepts: cardiac extracellular matrix remodeling after XXXX .

@entity1 @entity712 @entity5843 @entity19 @entity384 @entity35010 @entity397 @entity563 @entity583 @entity67
The cardiac extracellular matrix consists of a three-dimensional structural network of interstitial collagens to which other matrix components are attached. The main physiological functions of this network are to retain tissue integrity and cardiac pump function. Collagen deposition is controlled and can be modulated by hormonal factors, growth factors, cytokines, regulatory proteins and/or hemodynamic factors. Increased collagen deposition is a prerequisite to prevent dilatation of the infarcted area. Excessive accumulation of collagen leads to @entity67 and ultimately contributes to @entity712 . An appropriate balance of extracellular matrix synthesis and degradation is required for normal morphogenesis and maintenance of tissue architecture. A disbalance in the extracellular matrix turnover either by decreased matrix synthesis and/or increased degradation leads to less than normal extracellular matrix in the myocardium which in its turn may lead to @entity384 or even @entity397 . Extracellular matrix degrading enzymes expressed after @entity583 belong to the families of @entity563 and matrix metalloproteinases (MMPs) and are secreted as latent proenzymes that have to be activated. It is crucial to keep the activity of these enzymes under tight control by either influencing the synthesis, activation or inhibition by tissue inhibitors of MMPs (TIMPs) or @entity5843 . First studies using MMP inhibitors in experimental models of @entity583 seem to give attenuation of ventricular geometry but not always improvement of cardiac function. A central role in the activation of MMPs plays the plasminogen-plasmin system. Invasion of inflammatory cells and hitherto the rest of the wound healing cascade is inhibited in plasminogen or @entity35010 deficient @entity19 , most likely by the inhibition of MMP activity. Regulating the balance of extracellular matrix remodeling either by extracellular matrix synthesis or degradation might be one of the possible prevention mechanisms for @entity712 . But also regeneration of the vascular and cardiomyocyte network might be potential new treatments for @entity1 with @entity712 .
