Department of Ophthalmology, New Zealand National Eye Centre, Faculty of Medical and Health Sciences, The University of Auckland, Auckland 1142, New Zealand.
Buchanan Ocular Therapeutics Unit, Department of Ophthalmology, New Zealand National Eye Centre, Faculty of Medical and Health Sciences, The University of Auckland, Auckland 1142, New Zealand.
Int J Mol Sci. 2023 Jun 29;24(13):10866. doi: 10.3390/ijms241310866.
Dry eye disease (DED) is a multifactorial ocular surface disorder arising from numerous interrelated underlying pathologies that trigger a self-perpetuating cycle of instability, hyperosmolarity, and ocular surface damage. Associated ocular discomfort and visual disturbance contribute negatively to quality of life. Ocular surface inflammation has been increasingly recognised as playing a key role in the pathophysiology of chronic DED. Current readily available anti-inflammatory agents successfully relieve symptoms, but often without addressing the underlying pathophysiological mechanism. The NOD-like receptor protein-3 (NLRP3) inflammasome pathway has recently been implicated as a key driver of ocular surface inflammation, as reported in pre-clinical and clinical studies of DED. This review discusses the intimate relationship between DED and inflammation, highlights the involvement of the inflammasome in the development of DED, describes existing anti-inflammatory therapies and their limitations, and evaluates the potential of the inflammasome in the context of the existing anti-inflammatory therapeutic landscape as a therapeutic target for effective treatment of the disease.
干眼症（DED）是一种多因素的眼表疾病，源于多种相互关联的潜在病理，引发不稳定、高渗透压和眼表损伤的自我维持循环。相关的眼部不适和视觉障碍对生活质量产生负面影响。眼表炎症越来越被认为在慢性 DED 的病理生理学中发挥关键作用。目前可获得的现成抗炎药物可成功缓解症状，但通常无法解决潜在的病理生理机制。NOD 样受体蛋白-3（NLRP3）炎性小体途径最近被认为是眼表炎症的关键驱动因素，这在 DED 的临床前和临床研究中得到了报道。本综述讨论了 DED 与炎症之间的密切关系，强调了炎性小体在 DED 发展中的作用，描述了现有的抗炎治疗及其局限性，并评估了炎性小体在现有抗炎治疗领域中的潜力，作为治疗该疾病的有效治疗靶点。
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