Diabetic vascular disease and the potential role of macrophage glucose metabolism

Abstract

Cardiovascular complications remain the leading cause of mortality in adult human subjects with diabetes. Hyperglycemia has long been hypothesized to explain some of the effects of diabetes on cardiovascular complications caused by atherosclerosis, but a clear causative role for hyperglycemia has not been established. Recent studies in animal models indicate that glucose may play a role in diabetes-accelerated atherosclerosis by promoting pro-inflammatory responses in myeloid cells, which are key cell types in atherosclerosis. For example, monocytes and macrophages often take on a more pro-inflammatory phenotype in the setting of diabetes. Moreover, in-vitro studies demonstrate a connection between pro-inflammatory molecules and glucose metabolism in macrophages and dendritic cells. This review concerns the role of glucose metabolism in inflammatory macrophages, and their potential role in diabetic vascular disease. Further in-vivo studies, focusing on myeloid-specific effects of glucose metabolism as it relates to atherosclerosis, are needed to increase our understanding of the relationship between diabetes, myeloid cells, and cardiovascular disease.

Key words::

• Atherosclerosis
• diabetes
• glycolysis
• hyperglycemia
• inflammation
• macrophage
• mouse

Acknowledgements

This work was supported in part by NIH grants HL062887, HL092969 (Project 2), and HL097365 to KEB.

Declaration of interest: The authors state no conflict of interest and have received no payment in preparation of this manuscript.