自噬与炎症小体相互作用对干性年龄相关性黄斑变性影响的研究进展

Research progress on the effect of autophagy and inflammasome interaction on dry age-related macular degeneration

年龄相关性黄斑变性(AMD)是一种黄斑退行性疾病,多发于老年人,干性AMD是AMD的一种类型。本文对近年来相关文献进行综述,发现自噬与核苷酸结合寡聚化结构域样受体3(NLRP3)炎症小体之间存在相互作用,该机制对干性AMD的发病存在影响。NLRP3炎症小体是一种高蛋白复合物,激活后的炎症小体会活化半胱氨酸天冬氨酸蛋白酶-1(Caspase-1),介导视网膜色素上皮(RPE)细胞焦亡,导致干性AMD。促进自噬能抑制NLRP3炎症小体活化,保护RPE细胞免受炎症反应的损伤。抑制自噬能促进NLRP3炎症小体活化,加速玻璃膜疣出现和脂褐素沉积。激活后的NLRP3炎症小体会对自噬产生进一步的负向调节,这种相互作用造成的恶性循环影响着AMD的发生发展。本文旨在探究NLRP3炎症小体与自噬的相互作用在干性AMD中的意义,希望能借此提供治疗AMD的新的切入点。

Age-related macular degeneration(AMD)is a degenerative disease of macula.It mostly occurs in the elderly.Dry AMD is a type of AMD.This paper reviews the relevant docu‐ments in recent years,and discovers there is an interaction between autophagy and nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)inflammasome,which has an im‐pact on the pathogenesis of dry AMD.NLRP3 inflammasome is a high protein complex whose acti‐vation can activate cysteinyl aspartate specific protease-1(Caspase-1),mediate retinal pigment epithelial cell pyroptosis,leading to dry AMD.Promoting autophagy can inhibit the activation of NLRP3 inflammasome,protect RPE cells from the damage of inflammatory response.Inhibition of autophagy can promote the activation of NLRP3 inflammasome and accelerate the occurrence of vitreous warts and lipofuscin deposition.The activated NLRP3 inflammasome will further nega‐tively regulate autophagy.The vicious circle caused by this interaction affects the occurrence and development of AMD.This paper aims to explore the significance of the interaction between NLRP3 inflammasome and autophagy in dry AMD,hoping to provide a new entry point for the treatment of AMD.