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Clinical and Experimental Nephrology
Published in: Clinical and Experimental Nephrology 4/2013

01-08-2013 | Review Article

Role of the endothelial-to-mesenchymal transition in renal fibrosis of chronic kidney disease

Authors: Jianhua He, Yong Xu, Daisuke Koya, Keizo Kanasaki

Published in: Clinical and Experimental Nephrology | Issue 4/2013

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Abstract

All types of progressive chronic kidney disease (CKD) inevitably induce renal fibrosis, the hallmark of which is the activation and accumulation of a large number of matrix-producing fibroblasts or myofibroblasts. The activated fibroblasts or myofibroblasts are derived from diverse origins, such as residential fibroblasts, vascular pericytes, epithelial-to-mesenchymal transition (EMT), and bone marrow (circulating fibrocytes). Recently, endothelial-to-mesenchymal transition (EndMT) or endothelial-to-myofibroblast transition has also been suggested to promote fibrosis and is recognized as a novel mechanism for the generation of myofibroblasts. Similar to EMT, during EndMT, endothelial cells lose their adhesion and apical–basal polarity to form highly invasive, migratory, spindle-shaped, elongated mesenchymal cells. More importantly, biochemical changes accompany these distinct changes in cell polarity and morphology, including the decreased expression of endothelial markers and the acquisition of mesenchymal markers. This review highlights evidence supporting the important role of EndMT in the development of renal fibrosis in CKD and its underlying mechanisms, including novel biological significance of microRNA regulation.
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Metadata
Title
Role of the endothelial-to-mesenchymal transition in renal fibrosis of chronic kidney disease
Authors
Jianhua He
Yong Xu
Daisuke Koya
Keizo Kanasaki
Publication date
01-08-2013
Publisher
Springer Japan
Published in
Clinical and Experimental Nephrology / Issue 4/2013
Print ISSN: 1342-1751
Electronic ISSN: 1437-7799
DOI
https://doi.org/10.1007/s10157-013-0781-0

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