Moreover, the anti-fibrotic and anti-inflammatory effects of pirfenidone (used in the treatment of idiopathic pulmonary fibrosis) were not only connected with an inhibition of Col1 expression, but also with a suppression of Hsp47 expression in lung fibroblasts.43 In fact, pirfenidone significantly increases the protein expression levels of Cav-1 in lung tissue subjected to bleomycin-induced pulmonary fibrosis, and this Cav-1 induction strongly correlates with improvements in the lung fibrosis score.44 This evidence concerns the gene CAV1 and pulmonary fibrosis.