Experimental Pharmacotherapy for Dry Eye Disease: A Review.
Experimental Pharmacotherapy for Dry Eye Disease: A Review.
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DOI：
10.2147/jep.s237487
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发表时间：
2021
影响因子：
--
通讯作者：
Spampinato S
中科院分区：
文献类型：
--
作者：
Baiula M;Spampinato S
干眼症是一种复杂的多因素疾病，表现出异质性症状，包括干燥、畏光、眼部不适、刺激和烧灼感以及疼痛。这些症状会影响视觉功能，导致日常生活活动受限和工作效率降低，从而对生活质量产生严重影响。几种病理机制导致该疾病：蒸发性失水导致泪液稳态的损害和丧失，直接或间接地诱导炎症，形成自我延续的恶性循环。眼部免疫反应失调导致眼表损伤，这进一步促进了DED的发病机制。目前，DED治疗是基于一种灵活的逐步方法来确定最有益的干预措施。虽然大多数可用的治疗方法可以在一定程度上控制DED的一些体征和症状，但它们显示出显著的局限性，并且不能完全满足患有DED的患者的需求。本文综述了DED的新兴实验疗法。几种有前途的治疗策略正在开发中，目的是抑制炎症和恢复眼表微环境的稳态。来自早期临床试验的结果，测试EnaC阻断剂，TRPM 8激动剂或间充质干细胞在DED患者中的作用，特别期待证明它们对治疗DED的治疗价值。此外，DED，tivanisiran，IL-1 R拮抗剂EBI-005和SkQ 1的最先进的实验策略正在III期临床试验中进行测试，仍在进行中。尽管如此，尽管结果令人鼓舞，但仍需要进一步研究来证实新兴治疗DED的有效性和安全性。
Dry eye disease (DED) is a complex multifactorial disease showing heterogenous symptoms, including dryness, photophobia, ocular discomfort, irritation and burning but also pain. These symptoms can affect visual function leading to restrictions in daily life activities and reduction in work productivity with a consequently high impact on quality of life. Several pathological mechanisms contribute to the disease: evaporative water loss leads to impairment and loss of tear homeostasis inducing either directly or indirectly to inflammation, in a self-perpetuating vicious cycle. Dysregulated ocular immune responses result in ocular surface damage, which further contributes to DED pathogenesis. Currently, DED treatment is based on a flexible stepwise approach to identify the most beneficial intervention. Although most of the available treatments may control to a certain extent some signs and symptoms of DED, they show significant limitations and do not completely address the needs of patients suffering from DED. This review provides an overview of the emerging experimental therapies for DED. Several promising therapeutic strategies are under development with the aim of dampening inflammation and restoring the homeostasis of the ocular surface microenvironment. Results from early phase clinical trials, testing the effects of EnaC blockers, TRPM8 agonist or mesenchymal stem cells in DED patients, are especially awaited to demonstrate their therapeutic value for the treatment of DED. Moreover, the most advanced experimental strategies in the pipeline for DED, tivanisiran, IL-1R antagonist EBI-005 and SkQ1, are being tested in Phase III clinical trials, still ongoing. Nevertheless, although promising results, further studies are still needed to confirm efficacy and safety of the new emerging therapies for DED.