Inflammation and diabetes-accelerated atherosclerosis: myeloid cell mediators

被引：50
作者：
Kanter, Jenny E. [1 ]
Bornfeldt, Karin E. [1 ,2 ]
机构：
[1] Univ Washington, Dept Med, Div Metab Endocrinol & Nutr, Seattle, WA 98109 USA
[2] Univ Washington, Dept Pathol, Diabet & Obes Ctr Excellence, Seattle, WA 98109 USA
来源：
TRENDS IN ENDOCRINOLOGY AND METABOLISM | 2013年 / 24卷 / 03期
基金：
美国国家卫生研究院;
关键词：
acyl-CoA synthetase; arachidonic acid; eicosanoids; macrophage; monocyte; ACID-BINDING PROTEIN; GENE-EXPRESSION PROFILES; ACTIVATED RECEPTOR-GAMMA; APOLIPOPROTEIN-E; ALDOSE REDUCTASE; SEVERE HYPERCHOLESTEROLEMIA; UP-REGULATION; MICE LACKING; DEFICIENT; MACROPHAGES;
D O I：
10.1016/j.tem.2012.10.002
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Monocytes and macrophages respond to and govern inflammation by producing a plethora of inflammatory modulators, including cytokines, chemokines, and arachidonic acid (C20:4)-derived lipid mediators. One of the most prevalent inflammatory diseases is cardiovascular disease, caused by atherosclerosis, and accelerated by diabetes. Recent research has demonstrated that monocytes/macrophages from diabetic mice and humans with type 1 diabetes show upregulation of the enzyme, acyl-CoA synthetase 1 (ACSL1), which promotes C20:4 metabolism, and that ACSL1 inhibition selectively protects these cells from the inflammatory and proatherosclerotic effects of diabetes, in mice. Increased understanding of the role of ACSL1 and other culprits in monocytes/macrophages in inflammation and diabetes-accelerated atherosclerosis offers hope for new treatment strategies to combat diabetic vascular disease.
引用
收藏
页码：137 / 144
页数：8
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