Journal
CLINICAL AND EXPERIMENTAL NEPHROLOGY
Volume 17, Issue 4, Pages 488-497Publisher
SPRINGER
DOI: 10.1007/s10157-013-0781-0
Keywords
EndMT; EMT; Transforming growth factor-beta; MicroRNAs; Diabetes
Categories
Funding
- Kanazawa Medical University
- National Natural Science Foundation of China [30670980]
- Education Bureau of Sichuan Province [10ZA036]
- Ministry of human resources and social security of China [2009-26-366]
- Japan Society for the Promotion of Science [23790381]
- Japan Research Foundation for Clinical Pharmacology
- Daiichi-Sankyo Foundation of Life Science
- Ono Medical Research Foundation
- NOVARTIS Foundation (Japan) for the Promotion of Science
- Banyu Foundation
- Takeda Science Foundation
- Kanazawa Medical University [C2011-4, C2012-1, S2011-1, S2012-5]
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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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