Epithelial to Mesenchymal Transition (EMT) and Endothelial to Mesenchymal Transition (EndMT): Role and Implications in Kidney Fibrosis
Epithelial to Mesenchymal Transition (EMT) and Endothelial to Mesenchymal Transition (EndMT): Role and Implications in Kidney Fibrosis
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DOI：
10.1007/978-3-319-51436-9_13
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发表时间：
2017-01-01
期刊：
影响因子：
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通讯作者：
Youker, Keith
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文献类型：
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作者：
Cruz-Solbes, Ana S.;Youker, Keith
肾小管间质损伤是肾脏疾病的标志之一。特别是，间质纤维化在肾损伤的发展和进展中具有突出作用。产生胶原的成纤维细胞负责ECM沉积。然而，这些活化的成纤维细胞的来源尚不清楚。本章将详细讨论纤维化和肾脏疾病背景下上皮间质转化（EMT）和内皮间质转化（EndMT）的概念。简而言之，EMT和EndMT涉及细胞形状的变化，极性的丧失和与胶原蛋白产生增加相关的运动性增加。因此，提供了成纤维细胞的新来源。然而，关于肾脏疾病中EMT和EndMT的存在以及其在疾病发展中的负担和作用存在许多争议。本章的目的是提供一个概述的概念和促纤维化的途径，并提出证据，已发表的赞成和反对EMT和EndMT。
Tubulointerstitial injury is one of the hallmarks of renal disease. In particular, interstitial fibrosis has a prominent role in the development and progression of kidney injury. Collagen-producing fibroblasts are responsible for the ECM deposition. However, the origin of those activated fibroblasts is not clear. This chapter will discuss in detail the concept of epithelial to mesenchymal transition (EMT) and endothelial to mesenchymal transition (EndMT) in the context of fibrosis and kidney disease. In short, EMT and EndMT involve a change in cell shape, loss of polarity and increased motility associated with increased collagen production. Thus, providing a new source of fibroblasts. However, many controversies exist regarding the existence of EMT and EndMT in kidney disease, as well as its burden and role in disease development. The aim of this chapter is to provide an overview of the concepts and profibrotic pathways and to present the evidence that has been published in favor and against EMT and EndMT.