Renal studies provide an insight into cardiac extracellular matrix remodeling during health and disease

Abstract 

The remodeling of a heart ventricle after myocardial infarction involves numerous inflammatory mediators that may trigger a long-lasting and a highly fibrogenic process. Likewise, in the kidney, acute and chronic injuries may lead to abnormal extracellular matrix deposition and eventually lead to the loss of renal function. Major breakthroughs have emerged during the last ten years with respect to the pathophysiology of matrix remodeling. Epithelial and endothelial cells are plastic, and able to engage in epithelial (or endothelial)-to-mesenchymal transition (EMT or EndMT), thus actively contributing to the fibrogenesis. Members of the fibrinolytic system were demonstrated to possess unsuspected properties and interact with receptors and integrins on endothelial and epithelial cells. Finally, a notion that stem cells could integrate into damaged tissue has recently emerged, which likely contributes to the tissue repair. In many aspects, the kidney and the heart share many common injury mechanisms. We envision that some of them will be accessible as common therapeutic targets in the future.

Keywords: Extra-cellular matrix, Heart remodeling, Acute kidney injury, Fibrosis, Epithelial to mesenchymal transition, Endothelial to mesenchymal transition, Integrin, tPA, PAI-1, Transforming growth factor beta