期刊
THROMBOSIS AND HAEMOSTASIS
卷 121, 期 11, 页码 1464-1475出版社
GEORG THIEME VERLAG KG
DOI: 10.1055/s-0041-1726346
关键词
methylglyoxal; macrophage polarization; diabetes; metabolic activation
资金
- Collaborative Research Center Reactive metabolites and diabetic complications [1118]
- Helmholtz Future Topic AMPro
- Deutsche Forschungsgemeinschaft [Sonderforschungsbereich 1123 (B10)]
- Deutsches Zentrum fur Herz-Kreislauf-Forschung Junior Research Group Grant
The study demonstrates the impact of methylglyoxal on murine macrophages, resulting in inflammation and enhanced glycolysis. Treatment with MG upregulated a unique set of surface markers in macrophages, providing new targets for diagnosis or treatment under high MG conditions.
Metabolic complications in diabetic patients are driven by a combination of increased levels of nutrients and the presence of a proinflammatory environment. Methylglyoxal (MG) is a toxic byproduct of catabolism and has been strongly associated with the development of such complications. Macrophages are key mediators of inflammatory processes and their contribution to the development of metabolic complications has been demonstrated. However, a direct link between reactive metabolites and macrophage activation has not been demonstrated yet. Here, we show that acute MG treatment activated components of the p38 MAPK pathway and enhanced glycolysis in primary murine macrophages. MG induced a distinct gene expression profile sharing similarities with classically activated proinflammatory macrophages as well as metabolically activated macrophages usually found in obese patients. Transcriptomic analysis revealed a set of 15 surface markers specifically upregulated in MG-treated macrophages, thereby establishing a new set of targets for diagnostic or therapeutic purposes under high MG conditions, including diabetes. Overall, our study defines a new polarization state of macrophages that may specifically link aberrant macrophage activation to reactive metabolites in diabetes.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据