AIM:To determine the involvement of the transforming growth factor(TGF)-β with the development of experimental subretinal fibrosis in a mouse model.· METHODS:Subretinal fibrosis was induced by subretinal injection of macrophage-rich peritoneal exudate cells(PECs) and the local expression of TGF-β isoforms was assessed by quantitative real-time reverse transcription-polymerase chain reaction(RT-PCR) and enzyme-linked immunosorbent assay(ELISA) at various time points.In addition,we investigated the effect of TFG-β-neutralizing antibodies(TGF-β NAb) on subretinal fibrosis development.· RESULTS:TGF-β1 and TGF-β2 mRNA level was significantly elevated at day 2 after subretinal fibrosis induction and increased further to 5 and 6.5-fold respectively at day 5,reaching the peak.TGF-β3 mRNA was not detected in the present study.The result of ELSIA showed that active TGF-β1 and TGF-β2 levels were upregulated to 10-fold approximately,while total TGF-β1 and TGF-β2 levels were even upregulated more than 10-fold and more than 20-fold respectively in subretinal fibrosis mice in comparison with na?觙ve mice at day 5.TGF-β NAb resulted in a reduced subretinal fibrosis areas by 65% compared to animals from control group at day 7.· CONCLUSION:Our results indicate that TGF-β signaling may contribute to the pathogenesis of subretinal fibrogenesis and TGF-β inhibition may provide an effective,novel treatment of advanced and late-stage neovascular age-related macular degeneration. AIM: To determine the involvement of the transforming growth factor (TGF) -β with the development of experimental subretinal fibrosis in a mouse model. · METHODS: Subretinal fibrosis was induced by subretinal injection of macrophage-rich peritoneal exudate cells (PECs) and the local expression of TGF-β isoforms was assessed by quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) at various time points. -neutralizing antibodies (TGF-β NAb) on subretinal fibrosis development. · RESULTS: TGF-β1 and TGF-β2 mRNA level was significantly elevated at day 2 after subretinal fibrosis induction and further further to 5 and 6.5-fold respectively at day 5, reaching the peak.TGF-β3 mRNA was not detected in the present study. The results of ELSIA showed that active TGF-β1 and TGF-β2 levels were upregulated to 10-fold approximately, while total TGF-β1 and TGF-β2 levels were even upreg ulated more than 10-fold and more than 20-fold respectively in subretinal fibrosis mice in comparison with na? 觙 ve mice at day 5. TGF- [beta] NAb resulted in a reduced subretinal fibrosis areas by 65% ​​compared to animals from control group at day 7. · CONCLUSION: Our results indicate that TGF-β signaling may contribute to the pathogenesis of subretinal fibrogenesis and TGF-β inhibition may provide an effective, novel treatment of advanced and late-stage neovascular age-related macular degeneration.