Background Fuchs endothelial corneal dystrophy (FECD) is a common corneal endothelial disease. Its specific pathogenesis is still unclear, which limits the effect of clinical treatment.

Objective To explore the reliability and stability of establishing a delayed onset FECD animal model by ultraviolet A (UVA) irradiation of mouse cornea.

Methods A total of 36 female and 36 male mice were selected, with the right eyes exposed to 365 nm ultraviolet light to irradiate the cornea as the UVA group, while the left eyes served as the control group. Observations and sample collection were conducted at 1 week, 2 weeks, and 4 weeks post-modeling. The samples were used for immunofluorescence staining, hematoxylin-eosin (HE) staining, and transmission electron microscopy, with four samples in each group. The observation methods included the use of a slit-lamp microscope to assess corneal transparency, anterior segment optical coherence tomography (OCT) to measure corneal thickness, and in vivo confocal microscopy to examine the number and morphology of corneal endothelial cells.

Results Slit lamp photography and anterior segment OCT showed that the cornea of the mice in the UVA group was edematous, cloudy, and thickened (P<0.05). In vivo confocal microscopy results showed that the corneal endothelial cells of the mice were expanded, deformed, and decreased in number (P<0.05). In addition, the formation of vegetation “Guttae” was observed at the 4th week, which was one of the significant pathological features of FECD. The immunofluorescence staining (ZO-1/DAPI) results showed that mouse corneal endothelial cells were enlarged and deformed, and the junctions between cells were loosening. The decrease in the nuclear count of DAPI staining was significant (P<0.05); HE staining revealed that the corneal stroma collagen fibers of the UVA group were loose and edematous with enlarged gaps and corneal thickening, and endothelial cells were damaged. Transmission electron microscopy showed that the mitochondrial structure in the corneal endothelial cells of the UVA group was damaged, and the Descemet's membrane was thicker than that of the control group (P<0.05).

Conclusion This study confirms the feasibility of the animal model of late-onset FECD induced by UVA irradiation of mouse cornea, and the characteristics of corneal Descemet layer thickening and endothelial cell damage presented by this model are consistent with the pathological characteristics of FECDs.