首页|ULK1在炎症性疾病中的研究进展

ULK1在炎症性疾病中的研究进展

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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.
Research progress of ULK1 in inflammatory diseases
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.

ULK1ComplexAutophagyMitochondrial oxidative stressInflammation

刘婉婷、徐畅、王重阳、宋艺兰、李莉、延光海

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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

ULK1 复合体 自噬 线粒体氧化应激 炎症

国家自然科学基金吉林省科技厅项目

8197001820240404025ZP

2024

中国免疫学杂志
中国免疫学会,吉林省医学期刊社

中国免疫学杂志

CSTPCD北大核心
影响因子:0.926
ISSN:1000-484X
年,卷(期):2024.40(6)
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