The DOI matches its Crossref record; 21 of the 21 references it cites were found in a registry or an index.
TGF-β-Induced Endothelial-Mesenchymal Transition in Fibrotic Diseases
Open accessAbstract
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.
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Cites
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Cited by
Endothelial to Mesenchymal Transition in Cardiovascular Disease
Kovacic, J. C., Dimmeler, S., Harvey, R. P., Finkel, T., Aikawa, E., Krenning, G., & Baker, A. H. (2019) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2018.09.089 · Cited by 631
TGF‐β as a driver of fibrosis: physiological roles and therapeutic opportunities
Budi, E. H., Schaub, J. R., Decaris, M., Turner, S., & Derynck, R. (2021) · The Journal of Pathology · doi:10.1002/path.5680 · Cited by 292
Su, T., Yang, Y., Lai, S., Jeong, J., Jung, Y., McConnell, M., Utsumi, T., & Iwakiri, Y. (2021) · Cellular and Molecular Gastroenterology and Hepatology · doi:10.1016/j.jcmgh.2020.12.007 · Cited by 220
TGF-β as A Master Regulator of Aging-Associated Tissue Fibrosis
Ren, L.-L., Miao, H., Wang, Y.-N., Liu, F., Li, P., & Zhao, Y.-Y. (2023) · Aging and disease · doi:10.14336/ad.2023.0222 · Cited by 139
Inflammaging and Complement System: A Link Between Acute Kidney Injury and Chronic Graft Damage
Franzin, R., Stasi, A., Fiorentino, M., Stallone, G., Cantaluppi, V., Gesualdo, L., & Castellano, G. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.00734 · Cited by 93
Metadata
- Authors
- Pardali, E., Sanchez-Duffhues, G., Gomez-Puerto, M., & Ten Dijke, P.
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2017-10-17
- Volume
- 18
- Issue
- 10
- Pages
- 2157
- ISSN
- 1422-0067 (ISSN-L)
- OpenAlex
- W2766389820
- Cited by
- 360
- References
- 21
- FWCI
- 10.09
- Type
- journal article
- Language
- en
- Open access
- gold
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- Pardali, E., Sanchez-Duffhues, G., Gomez-Puerto, M., & Ten Dijke, P. (2017). TGF-β-Induced Endothelial-Mesenchymal Transition in Fibrotic Diseases. International Journal of Molecular Sciences. https://doi.org/10.3390/ijms18102157
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