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TRIM7对动脉粥样硬化泡沫细胞脂质积累的影响

赵艺琳 侯博文 蔡泽鸣 杨懿 朱丽华

医学新知2026,Vol.36Issue(4):421-427,7.
医学新知2026,Vol.36Issue(4):421-427,7.DOI:10.12173/j.issn.1004-5511.202502052

TRIM7对动脉粥样硬化泡沫细胞脂质积累的影响

The effect of TRIM7 on lipid accumulation in foam cells in atherosclerosis

赵艺琳 1侯博文 1蔡泽鸣 1杨懿 1朱丽华1

作者信息

  • 1. 武汉大学人民医院心内科(武汉 430060)
  • 折叠

摘要

Abstract

Objective To investigate the effect of TRIM7,an E3 ubiquitin protein ligase,on lipid accumulation in foam cells derived from mouse bone marrow-derived macrophages(BMDMs)and its mechanism.Methods Western blot and qRT-PCR were used to detect the expression changes of TRIM7 in BMDMs stimulated by oxidized low-density lipoprotein.Construct TRIM7 knockout BMDMs and TRIM7 overexpression THP-1 cell lines,and analyze the effect of TRIM7 on lipid metabolism of BMDMs through qRT-PCR,oil red staining,and total cholesterol content detection.Western blot was used to detect the phosphorylation levels of MAPK signaling pathway proteins in BMDMs after TRIM7 knockout.Immunoprecipitation detection of the interaction between TRIM7 and the upstream kinase TAK1 in the MAPK pathway.Results TRIM7 interacted directly with TAK1,TRIM7 knockout could enhance the phosphorylation activity of MAPK signaling pathway protein,up regulate the expression of CD36 and MSR1 and inhibit the expression of ABCA1,increase cholesterol uptake and reduce lipid excretion,and ultimately promote the formation of foam cells.Conclusion TRIM7 negatively regulates lipid accumulation in foam cells by inhibiting MAPK signaling pathway and scavenger receptor expression by directly binding to TAK1,which provides a potential new target for the treatment of atherosclerosis.

关键词

泡沫细胞/E3泛素蛋白连接酶/TRIM7/动脉粥样硬化

Key words

Foam cells/E3 ubiquitin-protein ligase/TRIM7/Atherosclerosis

分类

医药卫生

引用本文复制引用

赵艺琳,侯博文,蔡泽鸣,杨懿,朱丽华..TRIM7对动脉粥样硬化泡沫细胞脂质积累的影响[J].医学新知,2026,36(4):421-427,7.

基金项目

国家自然科学基金面上项目(82170455) (82170455)

医学新知

1004-5511

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