UV Protection in the Cornea: Failure and Rescue.
Thomas L A VolatierBjörn SchumacherClaus CursiefenMaria NotaraPublished in: Biology (2022)
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.
Keyphrases
- dna repair
- dna damage response
- circulating tumor
- cell free
- single molecule
- dna damage
- endothelial cells
- end stage renal disease
- oxidative stress
- high glucose
- cell death
- gene expression
- endoplasmic reticulum stress
- ejection fraction
- chronic kidney disease
- newly diagnosed
- soft tissue
- drug induced
- genome wide
- dna methylation
- cell cycle arrest
- cell proliferation
- radiation induced