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Int. J. Mol. Sci. 2017, 18(10), 2157; https://doi.org/10.3390/ijms18102157

TGF-β-Induced Endothelial-Mesenchymal Transition in Fibrotic Diseases

1
Department of Cardiovascular Medicine, University of Münster, 48149 Münster, Germany
2
Department of Molecular Cell Biology and Cancer Genomics Center Netherlands, Leiden University Medical Center, 2333 ZC Leiden, The Netherlands
*
Author to whom correspondence should be addressed.
Received: 15 September 2017 / Revised: 6 October 2017 / Accepted: 13 October 2017 / Published: 17 October 2017
(This article belongs to the Special Issue TGF-beta Family in Fibrosis and Cancer)
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Abstract

Fibrotic diseases are characterized by net accumulation of extracellular matrix proteins in affected organs leading to their dysfunction and ultimate failure. Myofibroblasts have been identified as the cells responsible for the progression of the fibrotic process, and they originate from several sources, including quiescent tissue fibroblasts, circulating CD34+ fibrocytes and the phenotypic conversion of various cell types into activated myofibroblasts. Several studies have demonstrated that endothelial cells can transdifferentiate into mesenchymal cells through a process termed endothelial- mesenchymal transition (EndMT) and that this can give rise to activated myofibroblasts involved in the development of fibrotic diseases. Transforming growth factor β (TGF-β) has a central role in fibrogenesis by modulating the fibroblast phenotype and function, inducing myofibroblast transdifferentiation and promoting matrix accumulation. In addition, TGF-β by inducing EndMT may further contribute to the development of fibrosis. Despite extensive investigation of the pathogenesis of fibrotic diseases, no effective treatment strategies are available. Delineation of the mechanisms responsible for initiation and progression of fibrotic diseases is crucial for the development of therapeutic strategies for the treatment of the disease. In this review, we summarize the role of the TGF-β signaling pathway and EndMT in the development of fibrotic diseases and discuss their therapeutic potential. View Full-Text
Keywords: endothelial cells; endothelial-mesenchymal transition; extracellular matrix; fibrosis; myofibroblasts; Smad; TGF-β signaling endothelial cells; endothelial-mesenchymal transition; extracellular matrix; fibrosis; myofibroblasts; Smad; TGF-β signaling
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Pardali, E.; Sanchez-Duffhues, G.; Gomez-Puerto, M.C.; ten Dijke, P. TGF-β-Induced Endothelial-Mesenchymal Transition in Fibrotic Diseases. Int. J. Mol. Sci. 2017, 18, 2157.

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