端粒通过抗氧化应激作用影响年龄相关性白内障的发病过程

目前认为氧化应激可能与年龄相关性白内障发病机制有关。端粒长度缩短与细胞衰老有关,氧化应激可加速端粒损伤及缩短。端粒酶具有维持端粒长度、提高细胞抗氧化应激及促进细胞增殖的作用。晶状体上皮细胞是少数几种具有端粒酶活性的成熟体细胞,端粒酶在其中主要起到抗氧化应激的细胞保护作用,而非促进细胞增殖。而端粒长度与白内障之间的关系存在种属特异性。总结氧化应激与端粒系统间的相互作用及其对年龄相关性白内障发生发展的影响,有助于理解年龄相关性白内障的发病机制并为其防治提供新思路。

Telomere influences the pathogenesis of age-related cataract through anti-oxidative stress

The pathogenesis of age-related cataracts remains unclear. Oxidative stress is considered associated with the occurrence of age-related cataract at present. Telomere length is the “molecular clock” for cell lifespan. Telomere shortening is associated with senescence of cells, and oxidative stress can accelerate telomeric damage and telomere shortening. Telomerase can maintain telomere length, increase the resistance to oxidative stress, and promote cell proliferation. Telomerase activity only exists in several somatic cell types, including lens epithelium. In lens epithelial cells, telomerase mainly improves cells’ resistance to oxidative stress, and protect cells from damage, rather than promote cell proliferation. Varying from animals and humans, the association between telomere length and cataract is species-specific. Therefore, an insight into the interaction of oxidative stress with the telomeric system and their influence on the pathogenesis of age-related cataracts is helpful for the treatment and prevention of age-related cataracts.(Int Rev Ophthalmol, 2020, 44：99-104)