Volatier Thomas, Schumacher Björn, Cursiefen Claus, Notara Maria
Department of Ophthalmology, Faculty of Medicine and University Hospital Cologne, University of Cologne, 62, 50937 Cologne, Germany.
Cologne Excellence Cluster for Cellular Stress Responses, Aging-Associated Diseases (CECAD) and Center for Molecular Medicine (CMMC), University of Cologne, Joseph-Stelzmann-Strasse 26, 50931 Cologne, Germany.
Biology (Basel). 2022 Feb 10;11(2):278. doi: 10.3390/biology11020278.
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.
紫外线（UV）照射会在所有直接暴露的组织中诱发DNA损伤。在人体中，有两个组织长期暴露于紫外线：皮肤和角膜。最常见的紫外线诱发的DNA损伤是环丁烷嘧啶二聚体（CPD），其可导致细胞凋亡或诱发肿瘤发生。透明的角膜缺乏皮肤的保护色素沉着，特别依赖核苷酸切除修复（NER）来去除紫外线诱发的DNA损伤。DNA损伤反应还会触发细胞内自噬机制，以清除角膜中的受损物质；尽管这些机制在与紫外线相关的疾病中有所涉及，但人们对它们的了解甚少。存在涉及诸如T4内切核酸酶V或光解酶等异种DNA修复酶的治疗方案，并且这些方案已广泛用于皮肤科。角膜领域缺乏类似的工具来解决光敏感患者（例如患有遗传疾病或近期接受移植组织的患者）的DNA损伤问题。
