Seetha Munisamy¹ , Hemaniswarri Dewi Dewadas², Uma Eswari Punchanathan³, Vaughn Alexei Ng Bansing¹, Lucas Cashev¹, Kavinash Selva Ganesan¹

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 endothelium-dependent 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.