ULK1在炎症性疾病中的研究进展
Research progress of ULK1 in inflammatory diseases
刘婉婷 1徐畅 1王重阳 1宋艺兰 1李莉 1延光海1
作者信息
- 1. 吉林省过敏性常见疾病免疫与靶向研究重点实验室,延边大学医学院,延吉 133002
- 折叠
摘要
UNC-51样激酶1(ULK1)是参与调节自噬启动的重要因子,ULK1通过自噬和线粒体氧化应激调节炎症细胞因子,参与了多种疾病的病理过程.ULK1及其复合体受雷帕霉素(mTOR)和AMP活化蛋白激酶(AMPK)调节启动自噬,从而对多种炎症性疾病产生不同影响.而在炎症性疾病中,线粒体氧化应激可使ULK1入核加速细胞凋亡.因此,ULK1在炎症性疾病中发挥不同的重要作用.例如,ULK1在哮喘中启动气道上皮细胞线粒体的自噬,在急性肝衰竭中参与线粒体氧化应激,在动脉粥样硬化中影响相关炎症因子,在糖尿病中调节自噬.本文从ULK1的生物学功能、在炎症性疾病中的影响和靶向药物的研究进展进行综述.
Abstract
UNC-51-like kinase 1(ULK1)is an important factor involved in regulating the initiation of autophagy.ULK1 regu-lates inflammatory cytokines through autophagy and mitochondrial oxidative stress,and is involved in the pathological processes of var-ious diseases.ULK1 and its complexes are regulated by rapamycin(mTOR)and AMP-activated protein kinase(AMPK)to initiate au-tophagy,thereby exerting differential effects on a variety of inflammatory diseases.In inflammatory diseases,mitochondrial oxidative stress can induce ULK1 into the nucleus to accelerate apoptosis.Therefore,ULK1 plays different important roles in inflammatory dis-eases.For example,ULK1 initiates airway epithelial mitochondrial autophagy in asthma,participates in mitochondrial oxidative stress in acute liver failure,affects related inflammatory factors in atherosclerosis,and modulates beneficial effects of autophagy in diabetes.This article reviews the biological function of ULK1,its impact on inflammatory diseases and the research progress of targeted drugs.
关键词
ULK1/复合体/自噬/线粒体氧化应激/炎症Key words
ULK1/Complex/Autophagy/Mitochondrial oxidative stress/Inflammation引用本文复制引用
基金项目
国家自然科学基金(81970018)
吉林省科技厅项目(20240404025ZP)
出版年
2024
国家科技期刊平台
NSTL
万方数据