PPAR-alpha activation suppresses the TGF-b- induced profibrotic response in lung IPF fibroblasts

The peroxisome proliferator-activated receptor-a (PPAR-a) has been an interesting target in different inflammation and fibrosis models in lung research. To evaluate the efficacy of PPAR-agonists, lung fibroblasts from control and IPF patients. PPARa induction suppressed the TGF-b1 mediated profibrotic response in IPF fibroblasts. In addition Treatment with PPAR alpha agonists significantly inhibited COL1A2 and reduced injury after TGF-b1 treatment of IPF fibroblasts. Moreover, PPAR-a agonist significantly inhibited the IPF fibroblast proliferation, and the TGF-b1 signalling pathway associated proinflammatory and fibrotic response. Therefore, we propose that the PPAR-a ligand alleviates fibrotic response by controlling inflammation, inhibiting TGF-b signalling, and may be useful for limiting exacerbations and progress of pulmonary fibrosis.