In this review, I discuss current knowledge of endothelial dysfunction in altered glucose how endothelial glucose metabolism contributes to cell function and how endothelial glucose transport is regulated in health and disease ( Figure 1).Įndothelial cells become dysfunctional in high glucose environments, which is connected to glucose metabolism and transport. Indeed, endothelial glucose response is important in micro- and macro-vascular diseases ranging from atherosclerosis to cancer to Alzheimer’s disease. Research has shown that glucose-induced endothelial dysfunction varies among different vessel types and in different vascular beds that endothelial glucose metabolism is critical to cell phenotype and function and that endothelial glucose transport is a regulated process. Endothelial cells take up glucose from the blood, which they then metabolize or transport to cells of the vascular wall and parenchymal tissue. Endothelial cells are exposed to varying blood glucose concentrations during pre- and post-prandial cycles. Future studies of endothelial glucose response should begin to integrate dysfunction, metabolism and transport into experimental and computational approaches that also consider endothelial heterogeneity, metabolic diversity, and parenchymal tissue interactions.ĭue to their location between blood and tissue, endothelial cells have a unique relationship with glucose. Increasing evidence from the blood-brain barrier and peripheral vasculature suggests that endothelial cells regulate glucose transport through glucose transporters that move glucose from the apical to the basolateral side of the cell. Finally, endothelial cells transport glucose to the cells of the blood vessel wall and to the parenchymal tissue. Research over the past decade highlighted how manipulation of endothelial glycolysis can be used to control angiogenesis and microvascular permeability in diseases such as cancer. Endothelial cells also metabolize glucose for their own energetic needs. More recently, non-coding RNA, extracellular vesicles, and sodium-glucose cotransporter-2 inhibitors were shown to affect glucose-induced endothelial dysfunction. Four classical dysfunction pathways were identified, which were later shown to result from the common mechanism of mitochondrial superoxide overproduction. Endothelial glucose-induced dysfunction was first studied in diabetic animal models and in cells cultured in hyperglycemia. The endothelial cell response to glucose plays an important role in both health and disease.
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