Journal
TRENDS IN ENDOCRINOLOGY AND METABOLISM
Volume 24, Issue 3, Pages 137-144Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tem.2012.10.002
Keywords
acyl-CoA synthetase; arachidonic acid; eicosanoids; macrophage; monocyte
Categories
Funding
- National Institutes of Health [HL062887, H1092969, HL097365]
- Diabetes Research Center at the University of Washington [P30 DK017047]
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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.
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