Cited by 175Nitric Oxide and Endothelin EffectsLipoproteins and Cardiovascular HealthCholesterol and Lipid Metabolism

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Effects of HMG-CoA Reductase Inhibitors on Endothelial Function: Role of Microdomains and Oxidative Stress

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Mason, R. Preston, Walter, Mary F., Jacob, Robert F.·2004·Circulation

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Abstract

Certain pleiotropic activities reported for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are related to reductions in cellular cholesterol biosynthesis and isoprenoid levels. In endothelial cells, these metabolic changes contribute to favorable effects on nitric oxide (NO) bioavailability. Given the essential role of NO in preserving vascular structure and function, this effect of statins is of considerable therapeutic importance. Statins have been demonstrated to restore endothelial NO production by several mechanisms, including upregulating endothelial NO synthase (eNOS) protein expression and blocking formation of reactive oxygen species. In this article, we will discuss additional ways in which statins restore endothelial NO production and improve endothelial function. (1) Statins modulate membrane microdomain formation, resulting in reduced expression of proteins that specifically inhibit eNOS activation. (2) Statins reduce sterol biosynthesis, thus interfering with the formation of pathologic microdomains, including cholesterol crystalline structures. This observation has important implications for plaque stabilization, as these microdomains contribute to cholesterol crystal formation and endothelial apoptosis. Finally, (3) statins improve endothelial function by interfering with oxidative stress pathways through both enzymatic and nonenzymatic mechanisms. The relationships between membrane microdomains, cholesterol biosynthesis, and endothelial function will be discussed.

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Authors: Mason, R. P., Walter, M. F., & Jacob, R. F.
Affiliations: From the Cardiovascular Division, Department of Medicine (R.P.M.), Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass; and the Cardiovascular Research Group (R.P.M., M.F.W., R.F.J.), Elucida Research LLC, Beverly, Mass.
Brigham and Women's Hospital (US)
Venue: Circulation
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2004-06
Volume: 109
Issue: 21_suppl_1
Pages: II34-41
ISSN: 0009-7322 (ISSN-L)
1524-4539
DOI: 10.1161/01.cir.0000129503.62747.03
OpenAlex: W2148580947
Cited by: 175
References: 82
Citations by year: 2026: 2 · 2025: 1 · 2024: 3 · 2022: 1 · 2021: 8 · 2020: 6 · 2019: 4 · 2018: 3 · 2017: 8 · 2016: 5 · 2015: 8 · 2014: 9 · 2013: 9 · 2012: 6
FWCI: 10.85
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Circulation (publishedVersion)
PubMed (publishedVersion)
Funders: American Heart Association
Pfizer
National Heart, Lung, and Blood Institute
National Eye Institute
Topics: Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
Keywords: statins, endothelial function, nitric oxide bioavailability, endothelial nitric oxide synthase, lipid rafts, cholesterol biosynthesis, terpenoids, cholesterol crystals, oxidative stress, reactive oxygen species, endothelial cell apoptosis, plaque stabilization
MeSH terms: Animals, Arteriosclerosis, Cholesterol, Crystallization, Endothelium, Vascular, Humans, Nitric Oxide, Oxidative Stress, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Membrane Microdomains

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Effects of HMG-CoA Reductase Inhibitors on Endothelial Function: Role of Microdomains and Oxidative Stress

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