Age-related macular degeneration (AMD), a degenerative disease affecting the retinal pigment epithelium (RPE) and photoreceptors in the macula, is the leading cause of central blindness in the elderly. AMD progresses to advanced stages of the disease, atrophic AMD (aAMD), or in 15% of cases "wet" or neovascular AMD (nAMD), associated with substantial vision loss. Whilst there has been advancement in therapies treating nAMD, to date, there are no licenced effective treatments for the 85% affected by aAMD, with disease managed by changes to diet, vitamin supplements, and regular monitoring. AMD has a complex pathogenesis, involving highly integrated and common age-related disease pathways, including dysregulated complement/inflammation, impaired autophagy, and oxidative stress. The intricacy of AMD pathogenesis makes therapeutic development challenging and identifying a target that combats the converging disease pathways is essential to provide a globally effective treatment. Interleukin-33 is a cytokine, classically known for the proinflammatory role it plays in allergic disease. Recent evidence across degenerative and inflammatory disease conditions reveals a diverse immune-modulatory role for IL-33, with promising therapeutic potential. Here, we will review IL-33 function in disease and discuss the future potential for this homeostatic cytokine in treating AMD.
摘要: 年龄相关性黄斑变性(AMD)为影响黄斑区视网膜色素上皮(RPE)和光感受器的退行性疾病, 是老年人中心性视力丧失的主要原因。当AMD进展到晚期, 例如萎缩性AMD (aAMD)或15%的“湿性”或新生血管性AMD (nAMD), 将伴有严重的视力丧失。虽然nAMD的治疗手段有了进步, 但迄今为止, 对于85%的aAMD患者, 尚没有有效的疗法, 只能通过改变饮食、补充维生素和定期监测来控制疾病。AMD的发病机制复杂, 涉及高度整合以及常见的年龄相关的疾病通路, 包括补体/炎症失调、自噬受损和氧化应激。AMD发病机制的复杂性使得治疗的发展具有挑战性, 确定一个与疾病融合的靶点对于提供全球有效的治疗是至关重要的。白细胞介素−33是一种细胞因子, 在过敏性疾病中起促炎作用。最近有关退行性疾病和炎症性疾病的证据显示, IL-33具有多种免疫调节作用, 具有很好的治疗潜力。在这里, 我们将回顾IL-33在疾病中的作用, 并讨论这种稳态细胞因子治疗AMD的未来潜力。.
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