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- W2967966052 abstract "Renal fibrosis has been regarded as the common pathway of end-stage renal failure. Understanding the fundamental mechanism that leads to renal fibrosis is essential for developing better therapeutic options for chronic kidney diseases. So far, the main abstractions are on the injury of tubular epithelial cells, activation of interstitial cells, expression of chemotactic factor and adhesion molecule, infiltration of inflammatory cells and homeostasis of ECM. However, emerging studies revealed that endothelial cells (ECs) might happen to endothelial-to-mesenchymal transition (EndMT) dependent and/or independent endothelial dysfunction, which were supposed to accelerate renal fibrosis and are identified as new mechanisms for the proliferation of myofibroblasts as well. In this chapter, we are about to interpret the role of ECs in renal fibrosis and analyze the related molecules and pathways of both EndMT and EndMT independent endothelial dysfunction." @default.
- W2967966052 created "2019-08-22" @default.
- W2967966052 creator A5018626803 @default.
- W2967966052 creator A5026834273 @default.
- W2967966052 creator A5056758184 @default.
- W2967966052 date "2019-01-01" @default.
- W2967966052 modified "2023-09-26" @default.
- W2967966052 title "Role of Endothelial Cells in Renal Fibrosis" @default.
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