S-Nitrosylation: Mechanistic Links between Nitric Oxide Signaling and Atherosclerosis
- PMID: 40772994
- DOI: 10.1007/s11883-025-01321-y
S-Nitrosylation: Mechanistic Links between Nitric Oxide Signaling and Atherosclerosis
Abstract
Purpose of review: 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.
Recent findings: 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.
Keywords: Atherosclerosis; Cardiovascular Disease; Nitric Oxide; S-nitrosylation.
© 2025. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
Conflict of interest statement
Declarations. Competing interests: The authors declare no competing interests. Human and Animal Rights and Informed Consent: No animal or human subjects by the authors were used in this study.
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