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Role of hyperosmolarity in the pathogenesis and management of dry eye disease: Proceedings of the ocean group meeting

机译:高渗在干眼病的发病机理和治疗中的作用:海洋小组会议记录

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Dry eye disease (DED), a multifactorial disease of the tears and ocular surface, is common and has a significant impact on quality of life. Reduced aqueous tear flow and/or increased evaporation of the aqueous tear phase leads to tear hyperosmolarity, a key step in the vicious circle of DED pathology. Tear hyperosmolarity gives rise to morphological changes such as apoptosis of cells of the conjunctiva and cornea, and triggers inflammatory cascades that contribute to further cell death, including loss of mucin-producing goblet cells. This exacerbates tear film instability and drives the cycle of events that perpetuate the condition. Traditional approaches to counteracting tear hyperosmolarity in DED include use of hypotonic tear substitutes, which have relatively short persistence in the eye. More recent attempts to counteract tear hyperosmolarity in DED have included osmoprotectants, small organic molecules that are used in many cell types throughout the natural world to restore cell volume and stabilize protein function, allowing adaptation to hyperosmolarity. There is now an expanding pool of clinical data on the efficacy of DED therapies that include osmoprotectants such as erythritol, taurine, trehalose and L-carnitine. Osmoprotectants in DED may directly protect cells against hyperosmolarity and thereby promote exit from the vicious circle of DED physiopathology.
机译:干眼病(DED)是眼泪和眼表的多因素疾病,很常见,并且对生活质量产生重大影响。泪液水流减少和/或泪液水相蒸发增加会导致泪液渗透压过高,这是DED病理学恶性循环中的关键一步。眼泪渗透压过高会引起诸如结膜和角膜细胞凋亡的形态变化,并引发炎症级联反应,进一步导致细胞死亡,包括产生粘蛋白的杯状细胞丢失。这加剧了泪膜的不稳定性,并驱动了使病情永久化的事件循环。对抗DED中眼泪高渗的传统方法包括使用低渗眼泪替代品,该替代品对眼睛的持续时间较短。对抗DED中眼泪高渗的最新尝试包括渗透保护剂,有机小分子,这些分子在整个自然世界中用于许多细胞类型,以恢复细胞体积并稳定蛋白质功能,从而适应高渗。现在,有关DED治疗功效的临床资料正在不断扩大,包括渗透保护剂,如赤藓糖醇,牛磺酸,海藻糖和L-肉碱。 DED中的渗透保护剂可以直接保护细胞免于高渗性,从而促进从DED生理病理学的恶性循环中退出。

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