2006
DOI: 10.1161/01.atv.0000193626.22269.45
|View full text |Cite
|
Sign up to set email alerts
|

Low-Density Lipoprotein Cholesterol Determines Oxidative Stress and Endothelial Dysfunction in Saphenous Veins From Patients With Coronary Artery Disease

Abstract: Endothelial dysfunction is associated with raised levels of superoxide and biomarkers of oxidative stress in saphenous veins from CAD patients. LDL cholesterol is a major determinant of endothelial dysfunction and oxidative stress in these patients. These results support intensive LDL cholesterol-lowering therapy as suggested by recent clinical trials.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

4
52
1

Year Published

2006
2006
2024
2024

Publication Types

Select...
7
2

Relationship

1
8

Authors

Journals

citations
Cited by 50 publications
(57 citation statements)
references
References 34 publications
4
52
1
Order By: Relevance
“…The studies so far performed using these methods show that NO plays a central role in the regulation of venous endothelial function, similarly to what it does for arterial endothelial function (33,34). Interestingly, what emerges from these studies is that conditions associated with arterial endothelial dysfunction, like hypertension, smoking, diabetes, coronary artery disease, heart failure and renal failure, are also characterised by a dysfunction of venous endothelium (30,31,(35)(36)(37)(38)(39)(40)(41)(42) …”
Section: Endothelial Dysfunction and Thrombosismentioning
confidence: 92%
“…The studies so far performed using these methods show that NO plays a central role in the regulation of venous endothelial function, similarly to what it does for arterial endothelial function (33,34). Interestingly, what emerges from these studies is that conditions associated with arterial endothelial dysfunction, like hypertension, smoking, diabetes, coronary artery disease, heart failure and renal failure, are also characterised by a dysfunction of venous endothelium (30,31,(35)(36)(37)(38)(39)(40)(41)(42) …”
Section: Endothelial Dysfunction and Thrombosismentioning
confidence: 92%
“…Superoxide and hydrogen peroxide stimulate mitogen activated protein kinases, specifically, serine threonine kinase/protein kinase B (Akt/PKB), leading to hypertrophy and increased survival of vascular smooth muscle cells [22] and trigger matrix metalloproteinases (MMP), the effects of which are discussed below [23]. Vascular superoxide production has been shown to correlate with aortic compliance [24], augmentation index [13] and endothelial reactivity [25,26]. Vascular NADPH oxidase activity has also been shown to negatively impact vasomotor response to endothelium-dependent agonists [26].…”
Section: Potential Mechanisms Of Inflammation-induced Arterial Stiffementioning
confidence: 99%
“…One of the first steps in atheroclerosis is the penetration of the arterial wall by chemically altered LDL particles (small, dense and/or oxidized). Once they have reached the arterial wall, these lipoproteins stimulate the recruitment of several leukocytes such as macrophages and Th2 lymphocytes [54, 55]. The binding and influx of such inflammatory cells is also dependent upon monocyte recruitment mediators such as P-selectin, E-selectin, vascular cell adhesion molecule-1 and intracellular cell adhesion molecule-1, of which the expression is made possible by circulating cytokines such as tumor necrosis factor-α (TNF-α), CRP and interleukin (IL)-1β [56, 57].…”
Section: What Are the Clinical Manifestations Of The Metabolic Syndrome?mentioning
confidence: 99%