Nitric oxide bioavailability dysfunction involves in atherosclerosis
Abstract
The pathological characteristics of atherosclerosis (AS) include lipid accumulation, fibrosis formation and atherosclerotic plaque produced in artery intima, which leads to vascular sclerosis, lumen stenosis and irritates the ischemic changes of corresponding organs. Endothelial dysfunction was closely associated with AS. Nitric oxide (NO) is a multifunctional signaling molecule involved in the maintenance of metabolic and cardiovascular homeostasis. NO is also a potent endogenous vasodilator and enters for the key processes that suppresses the formation vascular lesion even AS. NO bioavailability indicates the production and utilization of endothelial NO in organisms, its decrease is related to oxidative stress, lipid infiltration, the expressions of some inflammatory factors and the alteration of vascular tone, which plays an important role in endothelial dysfunction. The enhancement of arginase activity and the increase in asymmetric dimethylarginine and hyperhomocysteinemia levels all contribute to AS by intervening NO bioavailability in human beings. Diabetes mellitus, obesity, chronic kidney disease and smoking, etc., also participate in AS by influencing NO bioavailability and NO level. Here, we reviewed the relationship between NO bioavailability and AS according the newest literatures.
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Decreased NO bioavailability occurs in response to lipid infiltration, oxidative stress, and inflammatory factors, which play a vital role in endothelial dysfunction.
“Its decrease occurs in response to lipid infiltration, oxidative stress, and inflammatory factors, which play a vital role in endothelial dysfunction [153].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [153]
Obesity, diabetes mellitus, smoking, chronic kidney disease, and so on participate in the pathogenesis of atherosclerosis via a mechanism of changing NO bioavailability.
“Obesity, diabetes mellitus, smoking, chronic kidney disease, and so on participate in the pathogenesis of atherosclerosis via a mechanism of changing NO bioavailability [153].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [153]
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- Authors
- Chen, J.-Y., Ye, Z.-X., Wang, X.-F., Chang, J., Yang, M.-W., Zhong, H.-H., Hong, F.-F., & Yang, S.-L.
- Affiliations
- Nanchang University (CN)
- Corresponding author
- Hong, Fen-fang
- Yang, Shu-long
- Venue
- Biomedicine & Pharmacotherapy
- Publisher
- Elsevier BV
- Published
- 2018-01
- Volume
- 97
- Pages
- 423-428
- ISSN
- 0753-3322 (ISSN-L)
- OpenAlex
- W2765547578
- Cited by
- 216
- References
- 62
- Citations by year
- 2026: 18 · 2025: 35 · 2024: 27 · 2023: 29 · 2022: 25 · 2021: 29 · 2020: 27 · 2019: 17 · 2018: 7 · 2017: 2
- FWCI
- 1.78
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Biomedicine & Pharmacotherapy (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81260504, 81660151, 81660751)
- Key Research and Development Program of Jiangxi Province (20161BBG70067)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- nitric oxide bioavailability, atherosclerosis, endothelial dysfunction, oxidative stress, asymmetric dimethylarginine, hyperhomocysteinemia, arginase, vascular inflammation, diabetes mellitus, obesity, chronic kidney disease, smoking, lipid accumulation, atherosclerotic plaque
- MeSH terms
- Animals, Arginine, Biological Availability, Cardiovascular Diseases, Endothelium, Vascular, Humans, Nitric Oxide, Obesity, Smoking, Vasodilation, Oxidative Stress, Atherosclerosis
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