LRG1 promotes atherosclerosis by inducing macrophage M1-like polarization

• 成果类型: Article
• 署名作者: Wang, Juan; Wang, Jing; Zhong, Jiuchang; Liu, Hongbin; Li, Weiming; Chen, Mulei; Xu, Li; Zhang, Wenbin; Zhang, Ze; Wei, Zhizhong; Guo, Jia; Wang, Xinyu; Sui, Jianhua; Liu, Xingpeng; Zhang, Sitao; Wang, Xiaodong
• 署名单位: Capital Medical University; National Institute of Biological Sciences, Beijing; Tsinghua University
• 刊物名称: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
• ISSN/ISSBN: 0027-14890
• DOI: 10.1073/pnas.2405845121
• 发表日期: 2024-08-27
• 关键词: immunometabolism; inflammation; disease; biomarkers; monocyte; cells; jnk

摘要

Atherosclerosis is a chronic inflammatory disease of the arterial wall characterized by the accumulation of cholesterol- rich lipoproteins in macrophages. How macrophages commit to proinflammatory polarization under atherosclerosis conditions is not clear. Report here that the level of a circulating protein, leucine- rich alpha- 2 glycoprotein 1 (LRG1), is elevated in the atherosclerotic tissue and serum samples from patients with coronary ization through the activation of extracellular signal- regulated kinase 1/2 (ERK1/2) and delayed atherogenesis progression and reduced levels of macrophage- related proinflamM1- like polarization in vitro and conferred therapeutic benefits to animals with ApoE deficiency- induced atherosclerosis. LRG1 may therefore serve as an additional biomarker patients by mitigating the proinflammatory response of macrophages.