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J. Clin. Med. 2016, 5(4), 45; doi:10.3390/jcm5040045

Endothelial to Mesenchymal Transition (EndoMT) in the Pathogenesis of Human Fibrotic Diseases

1
Jefferson Institute of Molecular Medicine, Department of Dermatology and Cutaneous Biology, Thomas Jefferson University, 233 S. 10th Street, Suite 509 BLSB, Philadelphia, PA 19107, USA
2
Rheumatology Division, Department of Medicine, Thomas Jefferson University, 233 S. 10th Street, Suite 509 BLSB, Philadelphia, PA 19107, USA
*
Author to whom correspondence should be addressed.
Academic Editors: David A. Brenner, Tatiana Kisseleva and Jonas Fuxe
Received: 21 January 2016 / Revised: 18 March 2016 / Accepted: 6 April 2016 / Published: 11 April 2016
(This article belongs to the Special Issue Epithelial-Mesenchymal Transition)
View Full-Text   |   Download PDF [1288 KB, uploaded 11 April 2016]   |  

Abstract

Fibrotic diseases encompass a wide spectrum of clinical entities including systemic fibrotic diseases such as systemic sclerosis, sclerodermatous graft versus host disease, nephrogenic systemic fibrosis, and IgG4-associated sclerosing disease, as well as numerous organ-specific disorders including radiation-induced fibrosis, and cardiac, pulmonary, liver, and kidney fibrosis. Although their causative mechanisms are quite diverse, these diseases share the common feature of an uncontrolled and progressive accumulation of fibrous tissue macromolecules in affected organs leading to their dysfunction and ultimate failure. The pathogenesis of fibrotic diseases is complex and despite extensive investigation has remained elusive. Numerous studies have identified myofibroblasts as the cells responsible for the establishment and progression of the fibrotic process. Tissue myofibroblasts in fibrotic diseases originate from several sources including quiescent tissue fibroblasts, circulating CD34+ fibrocytes, and the phenotypic conversion of various cell types including epithelial and endothelial cells into activated myofibroblasts. However, the role of the phenotypic transition of endothelial cells into mesenchymal cells (Endothelial to Mesenchymal Transition or EndoMT) in the pathogenesis of fibrotic disorders has not been fully elucidated. Here, we review the evidence supporting EndoMT’s contribution to human fibrotic disease pathogenesis. View Full-Text
Keywords: Endothelial Mesenchymal Transition; EndoMT; fibrosis; fibrotic diseases; systemic sclerosis; idiopathic pulmonary fibrosis; endothelial cell; myofibroblast; collagen; extracellular matrix; transforming growth factor-β Endothelial Mesenchymal Transition; EndoMT; fibrosis; fibrotic diseases; systemic sclerosis; idiopathic pulmonary fibrosis; endothelial cell; myofibroblast; collagen; extracellular matrix; transforming growth factor-β
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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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MDPI and ACS Style

Piera-Velazquez, S.; Mendoza, F.A.; Jimenez, S.A. Endothelial to Mesenchymal Transition (EndoMT) in the Pathogenesis of Human Fibrotic Diseases. J. Clin. Med. 2016, 5, 45.

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