肾纤维化的机制.pptVIP

Mechanism of renal fibrosis li wei wei renal fibrosis is the final common pathway for nearly all forms of kidney disease that progress towards end-stage renal failure. As a sequel of inflammation and injury, humoral factors are released by infiltrating and resident renal cells that stimulate kidney tissues to produce extracellular matrix (ECM) molecules, like typeⅠ and Ⅲ collagens, fibronectin and proteoglycans. it is believed that overproduction of such ECM generates fibrosis, leading to the permanent loss of normal structure and function in the kidney. Mechanism of renal fibrosis 1. Epithelial to mesenchymal transition (EMT) and renal fibrosis 2. Hypoxia and renal fibrosis 3. Matrix degrading enzyme 4. SMAD family 1. epithelial to mesenchymal transition (EMT)  Epithelial to Mesenchymal Transition (EMT) constitutes the principal mechanism of renal fibrosis along with local and circulating cells. Epithelial to Mesenchymal Transition (EMT) is tubular epithelial cells which are transformed to mesenchymal fibroblasts migrating to adjacent interstitial parenchyma. Fibroblasts are the main source of interstitial matrix accumulation in various pathological states While the role of fibroblasts in renal fibrosis is generally accepted, there is a lot of ambiguity regarding the origin of these cells. innovative studies revealed that tubular epithelial cells could also exhibit fibroblast-like characteristics in various renal diseases, supporting the theory of the epithelial to mesenchymal transition (EMT). Therefore, by definition, tubular EMT is a process in which the tubular renal cells lose their phenotypical epithelial characteristics and acquire new ones, which are characteristics of the mesenchymal cells. So these cells exhibit a transformation capacity, after which they can produce extracellular matrix.