S-Nitrosylation: Mechanistic Links between Nitric Oxide Signaling and Atherosclerosis

This review explores current knowledge on the beneficial and detrimental roles of nitric oxide (NO) in vascular biology, with a particular focus on the emerging role of protein S-nitrosylation in the pathophysiology of atherosclerosis.

Major risk factors for atherosclerosis include hypercholesterolemia, low-density lipoprotein (LDL) oxidation, hyperglycemia, hyperhomocysteinemia, chronic inflammation, and obesity. Recent studies have shown that protein S-nitrosylation interacts with these risk factors, influencing atherogenesis either by promoting or inhibiting disease progression. Atherosclerosis is a chronic inflammatory disorder marked by the accumulation of plaques within arterial walls, arising from intricate interactions among endothelial cells, monocytes/macrophages, and vascular smooth muscle cells. Understanding the role of S-nitrosylation in regulating key cellular events-such as endothelial dysfunction, foam cell formation, and vascular smooth muscle cell proliferation-offers new insights into the molecular mechanisms underlying atherosclerosis. These insights may ultimately lead to the identification of novel therapeutic targets for cardiovascular disease.