In contrast, the TGF-beta1 vector caused a more severe and prolonged inflammatory response as well as localized collagen deposition, leading to severe and progressive fibrosis.
We conclude that TGF-beta1 concentration may predict the development of kidney graft fibrosis; early CsA withdrawal may achieve a reduction in chronic tubular and interstitial injury of cadaveric kidney allografts.
Transforming growth factor-beta1 (TGF-beta1) is generally considered to be the major or predominant isoform involved in fibrosis, with the roles of TGF-beta2 and -beta3 being less clear.
Aspidin PB, a novel natural anti-fibrotic compound, inhibited fibrogenesis in TGF-β1-stimulated keloid fibroblasts via PI-3K/Akt and Smad signaling pathways.
We show that local and transient TGF-beta1 overexpression induces homogenous, prolonged, and progressive pleural fibrosis without pleurodesis, associated with severe impairment of pulmonary function.
In conclusion, this strongly suggests that TGF-beta1 derived from tubular epithelial cells and some macrophages might be related to the development of renal interstitial fibrosis in HgCl2-treated BN rats.
TGF-beta(1) expression was significantly correlated with both hepatic fibrosis and the percentage of portal tracts showing histological abnormalities associated with CFLD.
In conclusion, an ongoing inflammatory process, the expression of TGF-beta 1, and proliferation of myofibroblasts within the valves have a potential role in the valvular fibrosis, calcification, and changes in the extracellular matrix that lead to the scarring sequelae of rheumatic heart disease.
These results show, for the first time to our knowledge, that TGF-beta1 is highly expressed in HCs and is directly involved in the pathogenesis of BM reticulin fibrosis in HCL.