巨噬细胞极化
加压器
巨噬细胞
核受体
卵清蛋白
炎症
免疫学
癌症研究
生物
转录因子
免疫系统
遗传学
基因
体外
作者
Chenchen Hou,Lifeng Yan,Ke Sun,Tianyu Zhou,Yuxin Zou,Weining Xiong,Sheng‐Zhong Duan
标识
DOI:10.1038/s41420-023-01724-3
摘要
Macrophage polarization plays an important role in asthma. Nuclear receptor corepressor 1 (NCOR1) plays an important role in metabolic and cardiovascular diseases by regulating the function of macrophages. The aim of this research was to examine the role and mechanism of macrophage NCOR1 in the development of asthma. We used ovalbumin (OVA) to induce macrophage NCOR1-deficient mice for asthma formation. Our results revealed that macrophage NCOR1 deficiency markedly enhanced allergic airway inflammation. In addition, NCOR1 deficiency in macrophages was found to enhance M2 polarization. Mechanistic studies suggested that NCOR1 promoted macrophage polarization by interacting with PPARγ, contributing to the pathogenesis of asthma. In conclusion, macrophage NCOR1 deficiency promoted the regulation of M2 programming by enhancing PPARγ expression to exacerbate asthma. Macrophage NCOR1 might be a potential target for the treatment of asthma.
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