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. 2014 Jul 16:58:13-9.
doi: 10.1016/j.ejps.2014.02.014. Epub 2014 Mar 12.

Effect of pirfenidone on proliferation, TGF-β-induced myofibroblast differentiation and fibrogenic activity of primary human lung fibroblasts

Enrico Conte  1 , Elisa Gili  2 , Evelina Fagone  2 , Mary Fruciano  2 , Maria Iemmolo  2 , Carlo Vancheri  2
Affiliations

Effect of pirfenidone on proliferation, TGF-β-induced myofibroblast differentiation and fibrogenic activity of primary human lung fibroblasts

Enrico Conte et al. Eur J Pharm Sci. .

Abstract

Pirfenidone is an orally active small molecule that has been shown to inhibit the progression of fibrosis in animal models and in patients with idiopathic pulmonary fibrosis. Although pirfenidone exhibits well documented antifibrotic and antiinflammatory activities, in vitro and in vivo, its molecular targets and mechanisms of action have not been elucidated. In this study, we investigated the effects of pirfenidone on proliferation, TGF-β-induced differentiation and fibrogenic activity of primary human lung fibroblasts (HLFs). Pirfenidone reduced fibroblast proliferation and attenuated TGF-β-induced α-smooth muscle actin (SMA) and pro-collagen (Col)-I mRNA and protein levels. Importantly, pirfenidone inhibited TGF-β-induced phosphorylation of Smad3, p38, and Akt, key factors in the TGF-β pathway. Together, these results demonstrate that pirfenidone modulates HLF proliferation and TGF-β-mediated differentiation into myofibroblasts by attenuating key TGF-β-induced signaling pathways.

Keywords: Fibrogenic activity; IPF; Lung fibroblasts; Pirfenidone; Proliferation.

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  • Pirfenidone for Idiopathic Pulmonary Fibrosis.
    Adams TN, Eiswirth C, Newton CA, Battaile JT. Adams TN, et al. Am J Respir Crit Care Med. 2016 Aug 1;194(3):374-6. doi: 10.1164/rccm.201602-0258RR. Am J Respir Crit Care Med. 2016. PMID: 27244589 No abstract available.

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