NADPH　oxidases　(NOXs)　are　important　in　the　pathophysiology　of　fibrotic　diseases.　The　expression　and　activity　of　NOXs　are　regulated　by　growth　factors,　including　transforming　growth　factor　(TGF-beta).　The　proliferation　of　retinal　pigment　epithelial　(RPE)　cells　following　epithelial-to-mesenchymal　transition　(EMT)　is　a　major　pathological　change　involved　in　proliferative　vitreoretinopathy　(PVR).　The　aim　of　the　present　study　was　to　determine　the　effects　of　the　novel　NOX　inhibitor　VAS2870　on　the　TGF-beta-dependent　expression　of　NOX4　and　associated　cellular　events　in　RPE　cells.　Cell　viability　was　examined　using　a　Cell　Counting　Kit-8　assay　and　cell　cycle　progression　was　detected　by　flow　cytometric　analysis.　Immunofluorescence　analysis　and　western　blot　analysis　were　performed　to　assess　EMT.　It　was　found　that　TGF-beta　increased　the　expression　of　NOX4　and　that　pre-incubation　with　VAS2870　eliminated　this　effect.　Additionally,　TGF-beta　promoted　RPE　migration　and　increased　EMT.　Pre-incubation　with　VAS2870　significantly　prevented　TGF-beta　2-induced　EMT　by　decreasing　the　levels　of　a-smooth　muscle　actin　and　E-cadherin,　and　also　inhibited　the　migratory　ability　of　the　RPE　cells,　as　demonstrated　by　scratch　assays.　Finally,　VAS2870　suppressed　the　proliferation　of　RPE　cells,　and　led　to　G(1)-phase　cell　cycle　arrest　and　a　significant　downregulation　of　the　expression　of　cyclin　D1.　In　conclusion,　the　pharmacological　inhibition　of　NOX　may　be　a　promising　tool　for　the　treatment　of　PVR.