Xu Weixiong, Chen Daniel, Zhou Hua-Lin
Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta University, Augusta, GA, 30912, USA.
Curr Atheroscler Rep. 2025 Aug 7;27(1):78. doi: 10.1007/s11883-025-01321-y.
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.
本综述探讨一氧化氮（NO）在血管生物学中的有益和有害作用的现有知识，特别关注蛋白质S-亚硝基化在动脉粥样硬化病理生理学中的新作用。
动脉粥样硬化的主要危险因素包括高胆固醇血症、低密度脂蛋白（LDL）氧化、高血糖、高同型半胱氨酸血症、慢性炎症和肥胖。最近的研究表明，蛋白质S-亚硝基化与这些危险因素相互作用，通过促进或抑制疾病进展来影响动脉粥样硬化的发生。动脉粥样硬化是一种慢性炎症性疾病，其特征是动脉壁内斑块的积累，由内皮细胞、单核细胞/巨噬细胞和血管平滑肌细胞之间的复杂相互作用引起。了解S-亚硝基化在调节关键细胞事件（如内皮功能障碍、泡沫细胞形成和血管平滑肌细胞增殖）中的作用，为动脉粥样硬化的分子机制提供了新的见解。这些见解最终可能导致确定心血管疾病的新治疗靶点。
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