Our　study　aimed　to　elucidate　the　mechanism　by　which　circTHADA　competitively　adsorbs　miR-494-3p　to　regulate　CASP1-mediated　endothelial　cell　(EC)　pyroptosis　in　diabetic　retinopathy　(DR).　To　be　specific,　we　used　high　glucose　(HG)-induced　human　retinal　microvascular　endothelial　cells　(HRMECs)　as　DR　cell　models　and　streptozotocin　(STZ)-treated　mice　as　DR　mouse　models.　The　expression　levels　of　circTHADA,　miR-494-3p,　CASP1,　NLRP3,　GSDMD-N　and　IL-1　beta　were　detected　and　flow　cytrometry　was　applied　to　measure　cell　pyroptosis　rate　and　dual　luciferase　reporter　assays　were　utilized　to　determine　the　direct　binding　sites.　As　a　result,　exacerbated　EC　pyroptosis　in　DR　was　detected　in　DR　cell　and　mouse　models.　Based　on　differentially　expressed　circRNA　profiles　by　microarray　and　experimental　verification,　circTHADA　was　filtered　and　identified　to　regulate　CASP1-mediated　EC　pyroptosis.　miR-494-3p　was　then　proven　to　be　involved　in　circTHADA-mediated　ceRNA　network　by　bioinformatics　analysis　and　experimental　verification.　Further　gain-　and　loss-of-function　experiments　and　rescue　experiments　revealed　the　function　of　the　circTHADA/miR-494-3p/CASP1　axis　in　pyroptosis.