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

Mason, R. Preston; Walter, Mary F.; Jacob, Robert F.

doi:10.1161/01.cir.0000129503.62747.03

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

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

DOI 10.1161/01.cir.0000129503.62747.03

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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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Statins and angiotensin type 1 receptor blockers lower oxidative stress and inflammation and thereby improve endothelial function.
“Statins and angiotensin type 1 receptor blockers have been shown to reduce oxidative stress and inflammation, improving endothelial function.”
From Effect of Atorvastatin and Irbesartan, Alone and in Combination, on Postprandial Endothelial Dysfunction, Oxidative Stress, and Inflammation in Type 2 Diabetic Patients (2005) · cites this paper as [18]
Statins and AT-1 receptor blockers are commonly prescribed to prevent cardiovascular disease and diabetic complications, and their ancillary effects have been attributed to strong intracellular antioxidant activity.
“Statins and angiotensin type 1 (AT-1) receptor blockers are widely used in preventing CVD and diabetic complications, and it has been suggested that many of their ancillary effects are due to strong intracellular antioxidant activity.”
From Effect of Atorvastatin and Irbesartan, Alone and in Combination, on Postprandial Endothelial Dysfunction, Oxidative Stress, and Inflammation in Type 2 Diabetic Patients (2005) · cites this paper as [18]
Statins and AT-1 receptor blockers exert antioxidant effects via distinct pathways.
“Statins and AT-1 receptor inhibitors work as antioxidant in different ways.”
From Effect of Atorvastatin and Irbesartan, Alone and in Combination, on Postprandial Endothelial Dysfunction, Oxidative Stress, and Inflammation in Type 2 Diabetic Patients (2005) · cites this paper as [18]
Statins and AT-1 receptor blockers protect endothelial function and reduce inflammation in diabetic and nondiabetic subjects, an effect convincingly attributed to their intracellular antioxidant activity.
“Statins and AT-1 receptor blockers protect endothelial function and reduce inflammation in diabetic and nondiabetic subjects, and these effects are convincingly mediated through their intracellular antioxidant activity.”
From Effect of Atorvastatin and Irbesartan, Alone and in Combination, on Postprandial Endothelial Dysfunction, Oxidative Stress, and Inflammation in Type 2 Diabetic Patients (2005) · cites this paper as [18]

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Statins as antiinflammatory and immunomodulatory agents: A future in rheumatologic therapy?
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Statin Therapy Reduces Future Risk of Lower-Limb Amputation in Patients With Diabetes and Peripheral Artery Disease
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Erythrocyte-derived microvesicles induce arterial spasms in JAK2V617F myeloproliferative neoplasm
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Ongoing clinical trials of the pleiotropic effects of statins
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Therapeutic Levels of the Hydroxmethylglutaryl-Coenzyme A Reductase Inhibitor Lovastatin Activate Ras Signaling via Phospholipase D2
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Cholesterol in Brain Development and Perinatal Brain Injury: More than a Building Block
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Atherosclerosis Regression, Vascular Remodeling, and Plaque Stabilization⁎⁎Editorials published in the Journal of the American College of Cardiologyreflect the views of the authors and do not necessarily represent the views of JACCor the American College of Cardiology.
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Treatment with pravastatin and fenofibrate improves atherogenic lipid profiles but not inflammatory markers in ACTG 5087
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Statins reduce relapse rate in Takayasu arteritis
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Models for Describing Relations Among the Various Statin Drugs, Low-Density Lipoprotein Cholesterol Lowering, Pleiotropic Effects, and Cardiovascular Risk††Conflicts of interest: In the past 2 years, Dr. Robinson has received grants from Abbott Laboratories, Abbott Park, Illinois, Astra-Zeneca, Wilmington, Delaware, Bristol-Myers Squibb, Princeton, New Jersey, GlaxoSmithKline, Pittsburgh, Pennsylvania, Hoffman La Roche, Basel, Switzerland, Merck & Company, West Point, Pennsylvania, Pfizer, New York, New York, Procter & Gamble, Cinncinnati, Ohio, Sankyo, Parsippany, New Jersey, Schering-Plough, Kenilworth, New Jersey, and Takeda Pharmaceuticals, Lincolnshire, Illinois and honoraria for education programs from Merck & Company, and has been a consultant and advisory board member for Merck Schering Plough.
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Fluvastatin ameliorates endotoxin induced multiple organ failure in conscious rats
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Statins restore ischemic limb blood flow in diabetic microangiopathy via eNOS/NO upregulation but not via PDGF-BB expression
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Assessment of endothelial function: comparison of the pulse wave response to β2‐adrenoceptor stimulation with flow mediated dilatation
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Comparison of Effects of Different Statins on Contrast‐Induced Acute Kidney Injury in Rats: Histopathological and Biochemical Findings
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Euphol from Euphorbia tirucalli Negatively Modulates TGF-β Responsiveness via TGF-β Receptor Segregation inside Membrane Rafts
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Simvastatin improves lysosome function via enhancing lysosome biogenesis in endothelial cells
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Effects of short term atorvastatin treatment on cerebral hemodynamics in CADASIL
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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 › Nitric Oxide and Endothelin Effects
Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
Health Sciences › Medicine › Surgery › 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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