A case-control was conducted to evaluate the associations of the polymorphisms of TGF-β1 receptor-associated protein 1 (TGFBRAP1) and TGF-β1 receptor 2 (TGFBR2) with type 2 diabetes mellitus (T2DM), and its genetic effects on diabetes-related miRNA expression. miRNA microarray chip was used to screen T2DM-related miRNA and 15 differential expressed miRNAs were further validated in 75 T2DM and 75 normal glucose tolerance (NGT).
Moreover, ANRIL overexpression caused myocardial fibrosis and myocardial cell apoptosis, and it increased the expression of the myocardial fibrosis-related proteins TGF-β1, collagen I and collagen III in the T2DM-MI mice.
Our results show that the liver of HFD fed model that resembles early T2DM pathology in mice, is more sensitive to DEN, by inducing both Wnt/β-catenin and TGF β1/Smads tumorigenic pathways.
Diabetic Foot Ulcer as a Cause of Significant Decline in the Renal Function Among South Indian Population With Type 2 Diabetes: Role of TGF-β1 and CCN Family Proteins.
These results indicated that pirfenidone intervention inhibited the epithelial-mesenchymal transition and pulmonary fibrosis in rat silicosis model, which effects may be related to the TGF-β1/smad pathway.
Together, these results suggest that activation of AMPK by WEL followed by reduction in TGFβ1/Raf-MAPK signaling pathways may have a therapeutic potential in pulmonary fibrosis.
The increase of miR-140 inhibited TGF-β1-induced pulmonary fibrosis, and H19 upregulation diminished the inhibitory effects of miR-140 on TGF-β1-induced pulmonary fibrosis, which was involved in the TGF-β/Smad3 pathway.
In conclusion, our study demonstrated that SIRT6 inhibited MWCNTs-induced EMT in BEAS-2B cells through TGF-β1/Smad2 signaling pathway, which depended on its deacetylase activity, and provided evidences that targeting SIRT6 could be a potential novel therapeutic strategy for MWCNTs-induced pulmonary fibrosis.
Studies have shown that transforming growth factor-β1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) functions as a central mediating process that contributes to PF.
The present study investigated the role of Nimbolide, an important active constituent of Neem in TGF-β1 induced in vitro and bleomycin induced in vivo model of pulmonary fibrosis, with a slight emphasis on regulation of fibrosis related autophagy.
Here, we aimed to investigate the chemical constituents and biological activities of Hypericum longistylum and detect whether the isolated compounds inhibit the TGF-β1/Smad3 signaling pathway to identify candidate compounds for the treatment of pulmonary fibrosis.
To assess the in vivo role of P311 in lung fibrosis, BLM was instilled into the lungs of P311-knockout mice, in which fibrotic changes were significantly decreased in tandem with a reduction in TGF-β1, -β2, and -β3 concentration/activity compared with BLM-treated wild-type mice.
Furthermore, WT mice receiving adoptive macrophages from TIM-3-TG mice also had more serious lung fibrosis and increased expression of TGF-β1 and IL-10 than those receiving macrophages from WT mice.