糖尿病中巨噬细胞激活和功能的活性氧（ROS）。
Reactive oxygen species (ROS) in macrophage activation and function in diabetes.
机构信息
Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, the Netherlands; The Institute of Transfusion Medicine and Immunology, Medical Faculty Mannheim, University of Heidelberg, Germany.
The Institute of Transfusion Medicine and Immunology, Medical Faculty Mannheim, University of Heidelberg, Germany; Laboratory for Translational Cellular and Molecular Biomedicine, Tomsk State University, Tomsk, Russia.
出版信息
Immunobiology. 2019 Mar;224(2):242-253. doi: 10.1016/j.imbio.2018.11.010. Epub 2018 Dec 1.
In a diabetic milieu high levels of reactive oxygen species (ROS) are induced. This contributes to the vascular complications of diabetes. Recent studies have shown that ROS formation is exacerbated in diabetic monocytes and macrophages due to a glycolytic metabolic shift. Macrophages are important players in the progression of diabetes and promote inflammation through the release of pro-inflammatory cytokines and proteases. Because ROS is an important mediator for the activation of pro-inflammatory signaling pathways, obesity and hyperglycemia-induced ROS production may favor induction of M1-like pro-inflammatory macrophages during diabetes onset and progression. ROS induces MAPK, STAT1, STAT6 and NFκB signaling, and interferes with macrophage differentiation via epigenetic (re)programming. Therefore, a comprehensive understanding of the impact of ROS on macrophage phenotype and function is needed in order to improve treatment of diabetes and its vascular complications. In the current comprehensive review, we dissect the role of ROS in macrophage polarization, and analyze how ROS production links metabolism and inflammation in diabetes and its complications. Finally, we discuss the contribution of ROS to the crosstalk between macrophages and endothelial cells in diabetic complications.
在糖尿病环境中，会诱导产生大量的活性氧（ROS）。这会导致糖尿病的血管并发症。最近的研究表明，由于糖酵解代谢转变，糖尿病单核细胞和巨噬细胞中 ROS 的形成加剧。巨噬细胞是糖尿病进展的重要参与者，并通过释放促炎细胞因子和蛋白酶来促进炎症。由于 ROS 是激活促炎信号通路的重要介质，肥胖和高血糖诱导的 ROS 产生可能有利于在糖尿病发病和进展期间诱导 M1 样促炎巨噬细胞。ROS 诱导 MAPK、STAT1、STAT6 和 NFκB 信号通路，并通过表观遗传（重新）编程干扰巨噬细胞分化。因此，为了改善糖尿病及其血管并发症的治疗，需要全面了解 ROS 对巨噬细胞表型和功能的影响。在当前的综合综述中，我们剖析了 ROS 在巨噬细胞极化中的作用，并分析了 ROS 产生如何将代谢与糖尿病及其并发症中的炎症联系起来。最后，我们讨论了 ROS 对糖尿病并发症中巨噬细胞和内皮细胞相互作用的贡献。
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