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Significance FECD is a genetic and female-predominant disorder which is the leading cause of corneal transplantation worldwide. There are no pharmacologic treatments for FECD; thus, there is a significant unmet need to improve the understanding of female prevalence in FECD pathogenesis. Herein, we reveal a physiologically relevant mechanism of UVA light causing DNA damage and inducing FECD, where greater DNA damage correlates with more severe FECD phenotype in females. Importantly, the sex-dependent effect of UVA is driven by the activation of CYP1B1, an enzyme which converts estrogen into metabolites that cause DNA damage. This study demonstrates an in vivo FECD model based on CE susceptibility to oxidative stress; furthermore, an antioxidant, NAC, restores UVA-induced changes, providing a potential therapeutic target.

Ultraviolet A light induces DNA damage and estrogen-DNA adducts in Fuchs endothelial corneal dystrophy causing females to be more affected