Old and New Biomarkers Associated with Endothelial Dysfunction in Chronic Hyperglycemia

Figure 1

Graphic representation of the mechanisms underlying endothelial function (a) and dysfunction (b). (b) Indicates the old (IL-6, CRP) and emerging (EVs, genomics, and metabolomics) biomarkers of vascular damage assessment. Nitric oxide (NO) production plays a central role in modulating endothelial function. NO is generated from the metabolism of l-arginine by the endothelial nitric oxide synthase (eNOS). In an inflammatory and prooxidant environment, as occurs in diabetes, the superoxide anion may quench NO, thereby reducing the efficacy of a potent endothelium-derived vasodilator system that participates in the general homeostasis of the vasculature (b). The consequent altered endothelial homeostasis is associated with the production of molecules involved in vascular damage and atherosclerotic plaque progression. vSMC: vascular smooth muscle cells; cGMP: cyclic guanosine monophosphate; EC: endothelial cell; NADPH: nicotinamide adenine dinucleotide phosphate (reduced form); NADP: nicotinamide adenine dinucleotide phosphate; eNOS: endothelial nitric oxide synthase; NO: nitric oxide; O₂-: superoxide anion; ONOO-: peroxynitrite; IL-6: interleukin-6; CRP: C-reactive protein; EVs: extracellular vesicles.

(a)

(b)