Second, although inhibition of the recruitment of inflammatory cells as well as TGF-β1, CTGF, α-SMA, and PAI-1 expression were observed during fasudil administration, the detailed mechanisms by which fasudil acts to prevent bleomycin-induced pulmonary fibrosis remain to be determined in the context of the pleiotropic effects of fasudil and the complex pathogenesis of pulmonary fibrosis. Here, CCN2 is linked to pulmonary fibrosis.