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作 者:黄志娟 周静[1] 林小珍 喻康莹 郑林峰 HUANG Zhi-juan;ZHOU Jing;LIN Xiao-zhen;YU Kang-ying;ZHENG Lin-feng(a.Department of Nephrology,the First Affiliated Hospital,Nanchang University,Nanchang 330006,China;b.Grade 2020,Medical Department of Graduate School,Nanchang University,Nanchang 330006,China;c.Grade 2021,Medical Department of Graduate School,Nanchang University,Nanchang 330006,China)
机构地区:[1]南昌大学第一附属医院肾脏内科,南昌330006 [2]南昌大学研究生院医学部,南昌330006
出 处:《南昌大学学报(医学版)》2022年第5期97-101,共5页Journal of Nanchang University:Medical Sciences
基 金:国家自然科学基金(81960678);江西省青年基金项目(20181BAB215010)
摘 要:NLRP3炎性体是固有免疫的重要组成成分,它可以被各种类型的病原体或危险信号激活,作为炎症反应的核心,参与免疫反应及各项疾病发生发展的过程。自噬溶酶体途径可以通过某些机制限制NLRP3炎性体引发的炎症反应,在延缓糖尿病、缺血再灌注损伤、脏器纤维化、痛风及各种肾脏疾病等炎症相关疾病的进展中起着重要作用,自噬-NLRP3炎性体途径可为炎症性疾病的新药研制提供新的思路。NLRP3 inflammasome is a vital component of intrinsic immunity.As the kernel of inflammatory response,it can be activated by various types of pathogens or danger signals,and is involved in immune response and the occurrence and development of many diseases.The autophagy-lysosome pathway plays a significant role in retarding diabetes,ischemia reperfusion injury,organ fibrosis,gout,nephropathy and other inflammatory diseases through inhibiting the inflammatory response triggered by NLRP3 inflammasome.Therefore,the autophagy-NLRP3 inflammasome pathway may provide new ideas for the development of new drugs for inflammatory diseases.
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