Following the combination of S100A8/A9 and TLR4, which was intended to produce cardiac fibrosis, the expression of α-SMA, collagen 1A1, and 3A1 mRNA was also enhanced in fibroblasts (31, 32).In pulmonary fibrosis, HSP90 and uric acid react with TLR2/4, aggravating the expression of TIMP-1 and the synthesis of fibronectin (33). This evidence concerns the gene ACTA1 and pulmonary fibrosis.