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- Title
TGF-β -Induced Endothelial-Mesenchymal Transition in Fibrotic Diseases.
- Authors
Pardali, Evangelia; Sanchez-Duffhues, Gonzalo; Gomez-Puerto, Maria Catalina; Dijke, Peter ten
- 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.
- Subjects
FIBROSIS; TRANSFORMING growth factors-beta; MESENCHYMAL stem cells; ENDOTHELIAL cells; MYOFIBROBLASTS; EXTRACELLULAR matrix proteins; THERAPEUTICS
- Publication
International Journal of Molecular Sciences, 2017, Vol 18, Issue 10, p2157
- ISSN
1661-6596
- Publication type
Article
- DOI
10.3390/ijms18102157