Role of Endothelial Cells in Renal Fibrosis

被引：11

作者：

Yang, Zhen ^{[1
]}

He, Li-Jie ^{[1
]}

Sun, Shi-Ren ^{[1
]}

机构：

[1] Air Force Med Univ, Dept Nephrol, Affiliated Hosp 1, Xian, Shaanxi, Peoples R China

来源：

RENAL FIBROSIS: MECHANISMS AND THERAPIES | 2019年 / 1165卷

关键词：

Endothelial cell; Renal fibrosis; EndMT; Endothelial dysfunction; HEDGEHOG-INTERACTING PROTEIN; TO-MESENCHYMAL TRANSITION; CHRONIC KIDNEY-DISEASE; GROWTH-FACTOR; STEM-CELLS; VASCULAR ENDOTHELIUM; MOLECULAR-MECHANISMS; OXIDATIVE STRESS; PROGENITOR CELLS; NITRIC-OXIDE;

D O I：

10.1007/978-981-13-8871-2_8

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 ; 100201 ;

摘要：

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.

引用

页码：145 / 163

页数：19

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