Atrophic age-related macular degeneration (AMD) is a progressive form with macular atrophy. Unfortunately, the mechanism of atrophic AMD progression is not fully revealed, and the effective remedy to improve patient’s visual acuity is none today. This study aims to explore a new therapeutic target for atrophic AMD. Microarray analysis of the retinal pigment epithelium (RPE)-choroid-sclera complex from sodium iodate (NaIO₃)-administered retinal degeneration model mice revealed that the expression of G protein-coupled receptor 35 (Gpr35) mRNA was markedly increased. This result was similar to that of an analysis using the NCBI Gene Expression Omnibus database, which showed a trend toward increased expression of Gpr35 in the macular RPE-choroid of atrophic AMD patients. NaIO₃-induced retinal degeneration model mice showed different severities depending on the dose of NaIO₃. Gpr35 mRNA level was markedly upregulated in RPE-choroid-sclera complexes treated with 40 mg/kg NaIO₃, whereas those treated with 20 mg/kg NaIO₃ showed an increasing but non-significant trend. Immunostaining images showed that GPR35 expression was observed around the RPE layer after treatment with 40 mg/kg NaIO₃ and was merged with macrophage/microglia marker F4/80. Interestingly, the GPR35 agonist cromolyn suppressed NaIO₃-induced RPE cell death. These findings suggest that GPR35 might be a novel potential therapeutic target for the pathological progression of atrophic AMD.