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Fig. 7 | Respiratory Research

Fig. 7

From: Pirfenidone attenuates lung fibrotic fibroblast responses to transforming growth factor-β1

Fig. 7

Relationship between pirfenidone’s effect on TGF-β1-stimulated fibroblast bioactivity in vitro and biomarkers of lung fibrosis. Comparison of the relationships between suppression of TGF-β1-induced gel contraction by pirfenidone and serum (a) KL-6 and (b) SP-D levels, and between suppression of TGF-β1-induced migration and (c) KL-6 and (d) SP-D levels. Symbols represent individual patients. Linear regression was used. P < 0.05 indicates a positive relationship between pirfenidone response to TGF-β1-stimulated fibroblast bioactivity in vitro and biomarkers of lung fibrosis. (e) Schematic showing the mechanism via which pirfenidone controls TGF-β1-induced changes in fibrotic lung fibroblasts. Lung fibroblasts are continually exposed to TGF-β1 via airway cells-fibroblasts interaction, which is regulated by mediators released by airway cells under inflammatory conditions, resulting in distinct phenotype of fibrotic fibroblasts. This high sensitivity to TGF-β1, along with upregulation of CTHRC1 and FHL2, leads to the development of fibrosis in fibrotic fibroblasts. Treatment with pirfenidone can effectively block this process

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