Purpose: To examine the effects and mechanism of action of fasudil on cytoskeletal polymerization, collagen synthesis and apoptosis in fibroblasts derived from human urethral scar tissue.Materials and Methods: Fibroblasts treated with or without transforming growth factor β1 (TGF-β1, 10 ng/mL) were incubated with fasudil (12.5, 25, 50 μmol/L) for 24 h. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were used to determine the expression of Arp2, Arp3, WASP and WAVE2. Collagen I and III protein levels were also evaluated by western blotting. The filamentous actin cytoskeleton was examined by immunofluorescence and epifluorescence microscopy. An Annexin V-FITC/Propidium Iodide staining assay was used to investigate apoptosis.Results: TGF-β1-dependent... induction of actin polymerization and collagen synthesis and promotion of apoptosis were dose-dependent. When compared with untreated controls, fasudil significantly decreased the expression of Arp2, Arp3, WASP, WAVE2, Collagen I and Collagen III in cells treated with or without TGF-β1. Fasudil also promoted apoptosis in cells, irrespective of TGF-β1 treatment.Conclusion Irrespective of TGF-β1 activation status, fasudil suppresses actin polymerization and collagen synthesis and induces apoptosis in human urethral scar fibroblasts via the Rho\ROCK signaling pathway.