MRC Human Genetics Unit, MRC Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road, EH4 2XU, Edinburgh, UK,
Adv Exp Med Biol. 2014;801:251-7. doi: 10.1007/978-1-4614-3209-8_32.
Age-related macular degeneration (AMD) is the leading cause of blindness worldwide, affecting an estimated 50 million individuals aged over 65 years.Environmental and genetic risk-factors implicate chronic inflammation in the etiology of AMD, contributing to the formation of drusen, retinal pigment epithelial cell dysfunction and photoreceptor cell death. Consistent with a role for chronic inflammation in AMD pathogenesis, several inflammatory mediators, including complement components, chemokines and cytokines, are elevated at both the local and systemic levels in AMD patients. These mediators have diverse roles in the alternative complement pathway, including recruitment of inflammatory cells, activation of the inflammasome, promotion of neovascularisation and in the resolution of inflammation. The utility of inflammatory biomarkers in assessing individual risk and progression of the disease is controversial. However, understanding the role of these inflammatory mediators in AMD onset, progression and response to treatment may increase our knowledge of disease pathogenesis and provide novel therapeutic options in the future.
年龄相关性黄斑变性(AMD)是全球致盲的主要原因,估计有 5000 万 65 岁以上的人受到影响。环境和遗传风险因素表明,慢性炎症与 AMD 的病因有关,导致玻璃膜疣的形成、视网膜色素上皮细胞功能障碍和光感受器细胞死亡。慢性炎症在 AMD 发病机制中的作用是一致的,几种炎症介质,包括补体成分、趋化因子和细胞因子,在 AMD 患者的局部和全身水平都升高。这些介质在替代补体途径中具有多种作用,包括招募炎症细胞、激活炎症小体、促进新生血管形成和炎症消退。炎症生物标志物在评估个体疾病风险和进展方面的作用存在争议。然而,了解这些炎症介质在 AMD 发病、进展和对治疗的反应中的作用,可以增加我们对疾病发病机制的认识,并为未来提供新的治疗选择。