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The Role of Endothelial Dysfunction in Aortic Aneurysms
Gerasimos Siasos1, Konstantinos Mourouzis, Evangelos Oikonomou
1Mikras Asias 75 str, 115 27, Athens, Greece. gsiasos@med.uoa.gr.
Current Pharmaceutical Design
|August 27, 2015
Summary
Abdominal aortic aneurysm (AAA) involves complex pathogenic mechanisms, including inflammation and endothelial dysfunction. Targeting endothelial cells offers potential for new pharmaceutical treatments for this vascular disease.
Area of Science:
- Vascular Biology and Pathology
- Cardiovascular Disease Research
Background:
- Abdominal aortic aneurysm (AAA) is a vascular disease developing independently of atherosclerosis, despite shared risk factors.
- Pathogenesis involves matrix metalloproteinase activation, tissue degradation, smooth cell changes, and inflammatory infiltration.
Purpose of the Study:
- To explore the role of endothelial cells in abdominal aortic aneurysm (AAA) development.
- To identify potential therapeutic targets within endothelial cell dysfunction pathways.
Main Methods:
- Review of pathogenic mechanisms in AAA, focusing on endothelial cell responses.
- Analysis of factors influencing endothelial cells, including oxidative stress and inflammatory mediators.
- Examination of endothelial dysfunction markers like flow-mediated dilation (FMD) and pulse wave velocity (PWV).
Main Results:
- Endothelial cells contribute to AAA via increased oxidative stress, impaired nitric oxide (NO) bioavailability, and expression of inflammatory molecules.
- Endothelial dysfunction and arterial stiffness are reflected in indices such as FMD and PWV.
- Current treatment for large AAA is primarily surgical, with limited pharmaceutical options.
Conclusions:
- Endothelial cell dysfunction is a key factor in abdominal aortic aneurysm (AAA) pathogenesis.
- Focusing on endothelial cells may lead to novel pharmaceutical treatments for AAA.
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