Transforming growth factor-β1 (TGF-β1) alters the fibroblast phenotype by promoting transdifferentiation into myofibroblasts, which exhibit the ability to promote collagen synthesis and extracellular matrix (ECM) deposition, thereby playing a significant role in the pathology of silicosis.
Our data suggest that RLX may inhibit TGF-β1-mediated fibrosis during the process of silicosis, providing evidence for the protective effect of RLX on silica-induced pulmonary fibrosis.
Down-regulation of TGF-beta 1 expression in macrophages by taurine and niacin could attenuate silica-induced pulmonary fibroblasts proliferation in vitro, which may be of therapeutic potential for early stage silicosis.
The aims of the current investigation were to determine whether functional polymorphisms in the tumor necrosis factor-alpha (TNF-alpha) gene at position -308; in the transforming growth factor-beta 1 (TGF-beta1) gene at positions -509, +869 (codon 10), and +915 (codon 25); in the interleukin-10 (IL-10) gene at position -1,082, -819 and -592; and in the intron 1 of the interferon-gamma (IFN-gamma) gene at position +874 are associated with silicosis and PTB.