UV-A–based intervention for mitigating myopia progression via retinal dopaminergic pathways in rabbits

The global rise in myopia, particularly among children and young adults, has stimulated increasing interest in environmental and light-based preventive strategies. This study investigated the protective effects of ultraviolet-A (UV-A) light exposure on myopia progression in a form-deprivation model and explored its potential mechanism via dopaminergic retinal signaling. In this experimental study, form-deprivation myopia (FDM) was induced in rabbits, which were randomly assigned to either a control group (n = 7) or a UV-A–treated group (375 nm, 12 h/day for 5 days; n = 6). Axial length, refraction, and ocular surface safety (Schirmer’s test and clinical observations) were evaluated before and after treatment. Retinal tissues were analyzed for tyrosine hydroxylase (TH) and dopamine receptors (D₁R and D₂R). Axial elongation was assessed within and between groups. UV-A–treated eyes demonstrated a shorter axial length and a greater hyperopic shift compared with controls (17.72 ± 0.14 mm vs. 23.12 ± 2.34 mm, p = 0.001; +4.58 ± 0.66 D vs. +2.64 ± 1.41 D, p = 0.001). Schirmer’s test revealed no significant differences (p = 0.40). TH and D₂R expression levels were significantly higher in the UV-A group (p = 0.013 and p = 0.009, respectively). Limitations of the study include the short experimental duration, small sample size, and the absence of a UV dose–response analysis. Overall, UV-A light exposure showed potential in inhibiting ocular axial elongation and reversing myopic shifts in a form-deprivation model, possibly through activation of retinal dopaminergic pathways, highlighting UV-A as a promising light-based intervention for myopia control.