Fig. 5.

Proposed mechanism by which T1D increases the risk of endothelial cell injury. This schematic diagram represents the events that follow diabetic hyperketonemia and hyperglycemia. An increase in ROS production leads to the upregulation of the downstream signaling pathways and an increase in the expression of adhesion molecules. This eventually causes the adhesion of circulating blood cells to the endothelium, followed by infiltration, and thereby increasing the risk of plaque formation and development of atherosclerosis. This study proposes that ketones induce ROS production by upregulating NOX.