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The role of nitric oxide in mediating endothelium function in diabetes
Abstract
Diabetes mellitus (DM) is one of the leading causes of death. It is associated with cardiovascular
diseases and impaired endothelial function, which is critical for cardiovascular health. Endothelial cells
in blood vessels release endothelium-derived factors (EDFs) which include endothelium-derived
relaxing factors (EDRFs) like prostacyclin, nitric oxide (NO), and endothelium-derived hyperpolarizing
factor (EDHF), which relax blood vessels, and endothelium contracting factors (EDCFs) like angiotensin
II, endothelin I and thromboxane A2, which cause contractions. Diabetes impairs endotheliumdependent
relaxation, largely mediated by NO. Several studies have demonstrated that NO acts as a
vasodilator which is essential in mediating endothelium-dependent relaxation. Diabetes treatments
today are largely centered on reducing blood sugar levels. However, it is important to understand that
endothelial dysfunction (ED) begins as soon as diabetes is diagnosed. This dysfunction is an early
warning sign of atherosclerosis, which progresses to cardiovascular disease. This review provides
insights into NO and endothelial dysfunction mechanisms, aiding the development of current and future
treatments.