Figure 1.

An overview of nitric oxide (NO) signalling in both healthy (left) and dysfunctional (right) endothelium. Healthy endothelium maintains physiological vascular function through the beneficial effects of NO. The endothelium maintains tight junctions and has an anti-inflammatory and antithrombotic phenotype. Laminar shear stress, insulin and acetylcholine stimulate eNOS to produce NO. The dysfunctional endothelium is characterised by decreased NO production, an inflammatory phenotype shown by increased expression of cell adhesion molecules (CAMs), increased permeability shown by increased migration of vascular monocytes and increased leucocyte infiltration. Instead of forming a dimer, eNOS becomes uncoupled, resulting in the production of reactive oxygen species (ROS) instead of NO. The reduced level of NO and increased ROS lead to the initiation and progression of atherosclerosis.