Figure 7
From: TRPV1-mediated UCP2 upregulation ameliorates hyperglycemia-induced endothelial dysfunction
Upregulation of UCP2 by TRPV1 activation attenuates hyperglycemia-induced ROS production in ECs. The increased metabolism of glucose due to intracellular hyperglycemia leads to the overproduction of NADH, a critical component of the superoxide-generating mechanism in endothelial cells. Upregulation of mitochondrial UCP2 in response to elevated superoxide levels plays an active role in the feedback regulation of reactive oxygen species production that is associated with chronic oxidative stress. Activation of the endothelial TRPV1 channel in endothelial cells by dietary capsaicin mediates the phosphorylation of PKA and upregulates UCP2, thus inhibiting the activity of NADPH and decreasing ROS production in ECs.