TGF-β signaling in fibrosis
By A. Biernacka, M. Dobaczewski, Nikolaos G. Frangogiannis. Growth Factors, 2011
1,062 citations recorded by the source corpus.
Transforming growth factor β (TGF-β) is a central mediator of fibrogenesis. TGF-β is upregulated and activated in fibrotic diseases and modulates fibroblast phenotype and function, inducing myofibroblast transdifferentiation while promoting matrix preservation. Studies in a wide range of experimental models have demonstrated the involvement of the canonical activin receptor-like kinase 5/Smad3 pathway in fibrosis. Smad-independent pathways may regulate Smad activation and, under certain conditions, may directly transduce fibrogenic signals. The profibrotic actions of TGF-β are mediated, at least in part, through induction of its downstream effector, connective tissue growth factor. In light of its essential role in the pathogenesis of fibrosis, TGF-β has emerged as an attractive therapeutic target. However, the pleiotropic and multifunctional effects of TGF-β and its role in tissue homeostasis, immunity and cell proliferation raise concerns regarding potential side effects that may be caused by TGF-β blockade. This minireview summarizes the role of TGF-β signaling pathways in the fibrotic response.
Subfields: Molecular Biology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/90ae05b3175f32e1b96f45fc4a7727083c4c8f57
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Citations in the corpus
- New insights into TGF-β/Smad signaling in tissue fibrosis. (2018, background): “tosis and differentiation, increase ECM production, maintain fibroblast viability, inhibit metalloproteinase production, and facilitate collagen degradation [26].”
- An Introduction to Proteoglycans and Their Localization (2012, background): “Signaling from TGF-β receptors leads fairly directly to transcriptional regulation of, for example, type I collagen genes (Penttinen et al. 1988; Biernacka et al. 2011).”