UV Protection in the Cornea: Failure and Rescue

Simple Summary The sun is a deadly laser, and its damaging rays harm exposed tissues such as our skin and eyes. The skin's protection and repair mechanisms are well understood and utilized in therapeutic approaches while the eye lacks such complete understanding of its defenses and therefore often lacks therapeutic support in most cases. The aim here was to document the similarities and differences between the two tissues as well as understand where current research stands on ocular, particularly corneal, ultraviolet protection. The objective is to identify what mechanisms may be best suited for future investigation and valuable therapeutic approaches. Ultraviolet (UV) irradiation induces DNA lesions in all directly exposed tissues. In the human body, two tissues are chronically exposed to UV: the skin and the cornea. The most frequent UV-induced DNA lesions are cyclobutane pyrimidine dimers (CPDs) that can lead to apoptosis or induce tumorigenesis. Lacking the protective pigmentation of the skin, the transparent cornea is particularly dependent on nucleotide excision repair (NER) to remove UV-induced DNA lesions. The DNA damage response also triggers intracellular autophagy mechanisms to remove damaged material in the cornea; these mechanisms are poorly understood despite their noted involvement in UV-related diseases. Therapeutic solutions involving xenogenic DNA-repair enzymes such as T4 endonuclease V or photolyases exist and are widely distributed for dermatological use. The corneal field lacks a similar set of tools to address DNA-lesions in photovulnerable patients, such as those with genetic disorders or recently transplanted tissue.