眼科新进展2025,Vol.45Issue(1) :60-65.DOI:10.13389/j.cnki.rao.2025.0012

线粒体损伤和NLRP3炎症小体信号在年龄相关性黄斑变性中的研究进展

Research progress in mitochondrial damage and NLRP3 inflammasome signa-ling in age-related macular degeneration

邹悦 李云琴 谭欣 蒋俊良
眼科新进展2025,Vol.45Issue(1) :60-65.DOI:10.13389/j.cnki.rao.2025.0012

线粒体损伤和NLRP3炎症小体信号在年龄相关性黄斑变性中的研究进展

Research progress in mitochondrial damage and NLRP3 inflammasome signa-ling in age-related macular degeneration

邹悦 1李云琴 1谭欣 1蒋俊良1
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作者信息

  • 1. 650021 云南省昆明市,云南大学附属医院(云南省第二人民医院,云南省眼科医院)
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摘要

年龄相关性黄斑变性(AMD)是一种导致严重视力丧失的眼病.该病症的关键病理特征之一是视网膜的神经炎症反应.NLRP3炎症小体在调节这种神经炎症中扮演着至关重要的角色.研究表明,在AMD的发展过程中,NLRP3炎症小体的激活与线粒体的损伤、活性氧的产生及线粒体DNA的异常释放紧密相关.因此,针对NLRP3炎症小体的抑制剂可能成为一种对AMD治疗极具潜力的新方法.本文对线粒体损伤与NLRP3炎症小体信号途径在AMD发病机制中的作用进行了全面综述,展望了这一领域的研究进展.

Abstract

Age-related macular degeneration(AMD)is a critical ophthalmic condition characterized by substantial vis-ual impairment.Retinal neuroinflammation is one of the fundamental pathophysiological features of AMD.The NOD-like re-ceptor protein 3(NLRP3)inflammasome plays a crucial role in regulating neuroinflammation.It has been demonstrated that the activation of NLRP3 inflammasome is closely correlated with mitochondrial dysfunction,the increased production of reactive oxygen species(ROS),and the anomalous expulsion of mitochondrial DNA in the progression of AMD.There-fore,inhibitors targeting the NLRP3 inflammasome may become a new approach with great potential for AMD treatment.This article rigorously examines the role of mitochondrial impairment and NLRP3 inflammasome signaling in the pathogene-sis of AMD,highlighting current research advancements and prospective trajectories in this evolving field.

关键词

年龄相关性黄斑变性/炎症小体/线粒体/神经炎症

Key words

age-related macular degeneration/inflammasome/mitochondrion/neuroinflammation

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出版年

2025
眼科新进展
新乡医学院

眼科新进展

CSTPCDCSCD北大核心
影响因子:0.961
ISSN:1003-5141
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