Objective：Our study aimed to probe the potential molecular mechanism of long non - coding RNA(lncRNA)VIM Antisense RNA 1(VIM-AS1)in diabetic retinopathy. Methods：LncRNA VIM-AS1，miR-497-5p and FBXW7 mRNA expressions were determined using qRT - PCR. The FBXW7 protein level was also detected using western blotting. The cell viability，migration and apoptosis were evaluated using CCK-8 assay，wound healing assay and flow cytometry analysis，respectively. Additionally，the binding relationships among lncRNA VIM-AS1，miR-497-5p and FBXW7 were verified by dual luciferase reporter assaies. Results：LncRNA VIM -AS1 and FBXW7 expressions were remarkably reduced in HG -treated ARPE - 19 cells，while miR - 497 - 5p was upregulated. LncRNA VIM - AS1 could upregulate the expression of FBXW7 by competitively binding to miR - 497 - 5p. LncRNA VIM - AS1 overexpression promoted cell proliferation and migration，and inhibited cell apoptosis in HG-induced ARPE-19 cells，while miR-497- 5p overexpression abolished the effects of lncRNA VIM -AS1 overexpression on HG -induced ARPE -19 cells. Furthermore，FBXW7 knockdown abrogated the effects of miR -497-5p inhibition on cell phenotypes of HG -treated ARPE -19 cells. Conclusion：LncRNA VIM-AS1 could promote the proliferation and migration，while inhibited cell apoptosis of HG-treated ARPE-19 cells by regulation of miR-497-5p/FBXW7 axis，suggesting that lncRNA VIM-AS1 might have great potential as therapeutic target for diabetic retinopathy