UCL Institute of Ophthalmology, University College London, London EC1V 9EL, UK.
Akari Therapeutics Plc, London EC1V 9EL, UK.
Cells. 2021 Feb 15;10(2):396. doi: 10.3390/cells10020396.
Retinal vascular diseases have distinct, complex and multifactorial pathogeneses yet share several key pathophysiological aspects including inflammation, vascular permeability and neovascularisation. In non-infectious posterior uveitis (NIU), retinal vasculitis involves vessel leakage leading to retinal enlargement, exudation, and macular oedema. Neovascularisation is not a common feature in NIU, however, detection of the major angiogenic factor-vascular endothelial growth factor A (VEGF-A)-in intraocular fluids in animal models of uveitis may be an indication for a role for this cytokine in a highly inflammatory condition. Suppression of VEGF-A by directly targeting the leukotriene B4 (LTB4) receptor (BLT1) pathway indicates a connection between leukotrienes (LTs), which have prominent roles in initiating and propagating inflammatory responses, and VEGF-A in retinal inflammatory diseases. Further research is needed to understand how LTs interact with intraocular cytokines in retinal inflammatory diseases to guide the development of novel therapeutic approaches targeting both inflammatory mediator pathways.
视网膜血管疾病具有独特、复杂和多因素的发病机制，但它们有几个关键的病理生理方面是共同的，包括炎症、血管通透性和新生血管形成。在非感染性后葡萄膜炎（NIU）中，视网膜血管炎涉及血管渗漏，导致视网膜增大、渗出和黄斑水肿。新生血管形成并不是 NIU 的常见特征，然而，在葡萄膜炎动物模型中检测到主要的血管生成因子-血管内皮生长因子 A（VEGF-A）-在眼内液中，可能表明这种细胞因子在高度炎症状态下发挥作用。通过直接靶向白三烯 B4（LTB4）受体（BLT1）途径抑制 VEGF-A 表明，在视网膜炎症性疾病中，白三烯（LTs）在启动和传播炎症反应中具有突出作用，与 VEGF-A 之间存在联系。需要进一步研究以了解 LTs 如何与眼内细胞因子相互作用，以指导针对炎症介质途径的新型治疗方法的开发。
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