肿瘤坏死因子-α在年龄相关性黄斑变性中的研究进展

Advances in the Study of Tumor Necrosis Factor-αin Age-Related Macular Degeneration

年龄相关性黄斑变性(AMD)疾病形成机制错综复杂,至今仍未有定论。大量实验数据验证了缺血、缺氧时的视网膜产生一系列反应,刺激了以TNF-α为代表的炎性细胞因子的异常表达,由此引发视网膜的免疫炎症反应、氧化应激反应等过程,以及影响血管生成与破坏的动态平衡,减弱RPE细胞功能等,促进AMD发生发展。现就TNF-α的结构,其在AMD疾病的中存在的依据,以及其如何在早中期形成玻璃膜疣,在中晚期的干性AMD中促进光感受器细胞丧失,在中晚期湿性AMD中调控VEGF,促使病理性CNV生成等的病情进展中发挥作用进行相关论述。

The pathogenesis of AMD is intricate and still inconclusive.Plenty of experimental data verify that the retina produces a series of responses during ischemia and hypoxia.It stimulates the abnormal expression of inflammatory cytokines represented by TNF-α.This triggers processes such as immune inflammatory response and oxidative stress in the retina,as well as affecting the dynamic balance of angiogenesis and destruction,and weakening RPE cell function,which promote the development of AMD.This article discusses the structure of TNF-α,the evidence for the presence of TNF-αin AMD,and how it plays a role in the formation of vitreous membrane verruca in the early and middle stages,promoting the loss of photoreceptor cells in the middle and advanced dry AMD,regulating VEGF in the middle and advanced wet AMD,promoting the formation of pathological CNV and other disease progression are discussed.