首页|细胞衰老和衰老相关分泌表型在年龄相关性黄斑变性发病和治疗中的研究进展

细胞衰老和衰老相关分泌表型在年龄相关性黄斑变性发病和治疗中的研究进展

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年龄相关性黄斑变性(AMD)是我国主要的不可逆致盲性疾病。目前AMD的发病机制尚不完全明确。在各种应激下,细胞衰老被激活,端粒缩短、线粒体功能障碍、DNA损伤等,并释放多种衰老相关分泌表型因子。细胞衰老通过多种途径与AMD的发病机制有关,并促进慢性炎症和AMD的发生和发展。氧化应激、脂褐素、β-淀粉样蛋白、膜攻击复合物等相关的发病机制是目前的研究热点。环磷酸鸟苷-腺苷合成酶。干扰素刺激因子通路是早期AMD发生和发展的重要信号通路,为AMD的治疗提供了研究方向。目前选择性靶向诱导衰老细胞凋亡的抗衰老药物在AMD的治疗中表现出巨大潜能,新技术与细胞衰老的结合可以为AMD的治疗提供新的切入点,通过抗细胞衰老途径干预AMD的治疗具有广阔的应用前景。
Research progress on cellular senescence and senescence-associated secretory phenotype in pathogenesis and treatment of age-related macular degeneration
Age-related macular degeneration(AMD)is one of the leading irreversible causes of blindness in China.The pathogenesis of AMD is not fully understood at present.Under various stress conditions,cellular senescence is activated,characterized by telomere shortening,mitochondrial dysfunction,DNA damage,and the release of various senescence-related secretory phenotype factors.Senescence is implicated in the pathogenesis of AMD through multiple pathways,contributing to chronic inflammation and the onset and progression of AMD.Mechanisms such as oxidative stress,lipofuscin,β amyloid protein and the membrane attack complex have become hotspots of study in the pathogenesis of AMD.The cyclic guanosine phosphate-adenosine synthase-interferon stimulating factor synthase-stimulator of interferon gene pathway has emerged as a critical signaling pathway in the early development of AMD,providing direction for further research on AMD.Currently,senolytics,selective agents targeting the induction of senescent cell apoptosis,show significant potential in the treatment of AMD.The integration of new technologies with cellular senescence may offer a novel approach to AMD treatment,and intervening in the AMD treatment through anti-cellular senescence pathways holds promising prospects.

Age-related macular degenerationSenescenceOxidative stressInflammationReview

李雨晨、许译丹、赵峰、陈力迅

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南京医科大学第三临床医学院,南京 211166

南京市第一医院眼科,南京 210006

年龄相关性黄斑变性 衰老 氧化应激 炎症 综述

2024

中华眼底病杂志
中华医学会

中华眼底病杂志

CSTPCD北大核心
影响因子:0.928
ISSN:1005-1015
年,卷(期):2024.40(3)
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