首页|外泌体携带毒性蛋白在神经退行性疾病传播中的作用

外泌体携带毒性蛋白在神经退行性疾病传播中的作用

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外泌体(exosomes)是细胞外囊泡的一类亚型,由内体衍生并通过膜融合胞吐释放.外泌体介导细胞间信息通讯,在机体多种生理和病理过程中发挥重要作用.因其具有免疫原性低、可介导生物活性物质长距离运输等特点,外泌体被视为药物的理想生物载体.工程化的外泌体可增强药物递送的靶向性,因此外泌体靶向药物递送的研究极具前景.但部分研究指出外泌体在患病机体中发挥促进病理进程的作用,例如肿瘤细胞分泌的外泌体可以"迷惑"免疫细胞或通过改善微环境促进肿瘤增殖和迁移.在神经退行性疾病中外泌体通过促进炎性反应和致病蛋白的扩散等方式加重病程.本文通过综述外泌体携带毒性致病蛋白介导神经退行性疾病的进展和病理传播,为神经退行性疾病的发生发展提供新的见解,为外泌体工程化改造和临床应用提出警示和建议.
The Role of Exosomes Containing Toxic Proteins in the Pathological Propagation of Neurodegenera-tive Diseases
Exosomes are a subtype of extracellular vesicles derived from endosomes and released by membrane fusion and exocytosis.Exosome-mediated intercellular communication plays a criti-cal role in multiple physiological and pathological processes.Due to their low immunogenicity and ability to mediate long-distance transport of bioactive substances,exosomes are considered ideal biological carriers for drugs.Engineered exosomes can improve the targeting of drug delivery,making research on exosome-based drug delivery exceedingly promising.However,some studies have indicated that exosomes can facilitate pathological processes in diseased organisms.For in-stance,exosomes secreted by tumor cells can"mislead"immune cells or establish a favorable mi-croenvironment,thus promoting tumor proliferation and migration.In neurodegenerative disea-ses,exosomes exacerbate the disease by promoting inflammatory responses and the spread of pathogenic proteins.This article reviews the development and pathological propagation of neuro-degenerative diseases mediated by exosomes carrying toxic pathogenic proteins,offering new insights into the occurrence and development of neurodegenerative diseases,as well as cautions and recommendations for exosome engineering and clinical applications.

exosomesneurodegenerative diseasestoxic proteinastrocytesneuron

孟昱含、邹明新

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宁夏理工学院,石嘴山 753000

内蒙古科技大学包头师范学院,包头 014030

外泌体 神经退行性疾病 毒蛋白 星形胶质细胞 神经元

内蒙古自治区高等学校科研项目内蒙古自治区在线开放课程建设项目内蒙古科技大学包头师范学院教学改革项目

NJZY18384BSJG21Y013

2024

生理科学进展
中国生理学会,北京大学

生理科学进展

CSTPCD北大核心
影响因子:0.635
ISSN:0559-7765
年,卷(期):2024.55(2)
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