中性粒细胞胞外陷阱
自噬
羟基氯喹
医学
免疫学
免疫系统
HIF1A型
系统性红斑狼疮
红斑狼疮
缺氧(环境)
炎症
促炎细胞因子
细胞凋亡
内科学
生物
血管生成
抗体
化学
2019年冠状病毒病(COVID-19)
生物化学
疾病
有机化学
氧气
传染病(医学专业)
作者
Mingfang Li,Luobei Weng,Datang Yu,Guoxiang Yang,Jin Hao
摘要
Abnormal death of neutrophils and the subsequent ineffective clearance of cell fragments result in production of autoantigens that can lead to systemic lupus erythematosus (SLE). Excessive formation of neutrophil extracellular traps (NETs) can trigger the synthesis of pro-inflammatory cytokines such as type I interferons, leading to tissue damage and immune dysfunction in SLE patients. In this study, we found that a decrease in neutrophil counts in the peripheral blood was correlated with clinical parameters in SLE patients. Patients with low neutrophil counts had high renal activity index and chronicity index scores. NET formation and neutrophil autophagy in SLE patients were increased. The autophagy inhibitor hydroxychloroquine was shown to restrict NET formation. Using comprehensive bioinformatics analysis, we found that the expression of the autophagy-related gene, hypoxia-inducible factor 1A (HIF1A), was enhanced in peripheral neutrophils and in the renal glomeruli in SLE patients. Targeting HIF1A could be a potential therapeutic approach for SLE.
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