摘要
细胞焦亡是由GSDM(Gasdermin)家族蛋白介导的程序性细胞死亡方式。年龄相关性黄斑变性(AMD)是老年人不可逆性视力丧失的主要原因,其病理机制复杂,涉及慢性炎症、氧化应激、补体异常激活及视网膜色素上皮(RPE)细胞功能障碍等。近年研究表明,细胞焦亡通过激活核苷酸结合寡聚化结构域样受体(NLR)炎症小体(如NLRP3)及GSDM蛋白(如GSDMD、GSDME),在AMD的RPE细胞损伤、脉络膜新生血管形成及炎症放大中扮演关键角色。未来研究需深入探索不同焦亡通路在干性与湿性AMD中的特异性作用,并开发靶向焦亡关键分子的高效、特异性抑制剂,为AMD的防治提供新策略。
Pyroptosis is a form of programmed cell death mediated by Gasdermin(GSDM)family proteins.Age-related macular degeneration(AMD),a leading causeof irreversible vision loss in the elderly,involves complex pathogenesis including chronic inflammation,oxidative stress,abnormal complement activation,and retinal pigment epithelium(RPE)dysfunction.Recent studies have shown that cell pyroptosis plays a key role in RPE cell damage,choroidal neovascularization,and inflammation amplification in AMD by activating nucleotide binding oligomeric domain like receptors(NLR)inflammasomes(such as NLRP3)and GSDM proteins(such as GSDMD,GSDME).Future research needs to deeply explore the specific roles of different pyroptosis pathways in dry and wet AMD,and develop efficient and specific inhibitors targeting key pyroptosis molecules to provide new strategies for the prevention and treatment of AMD.
作者
高景昭
许嘉洋
张天资
GAO Jingzhao;XU Jiayang;ZHANG Tianzi(School of Clinical Medicine,Inner Mongolia University for Nationalities,Tongliao O28000 China;Department of Ophthalmology,Tangshan Guangming Hospital,Tangshan 064000,China;Department of Ophthalmology,Inner Mongolia University for Nationalities Affiliated Hospital,Tongliao 028000,China)
出处
《医学综述》
2025年第21期2586-2592,共7页
Medical Recapitulate
