Projects / Programmes
Atherosclerosis and inflammation
| Code |
Science |
Field |
Subfield |
| 3.06.00 |
Medical sciences |
Cardiovascular system |
|
| Code |
Science |
Field |
| B001 |
Biomedical sciences |
General biomedical sciences |
| B530 |
Biomedical sciences |
Cardiovascular system |
atherosclerosis, inflammation, endothelial dysfunction, adhesion molecules
Researchers (24)
Organisations (1)
Abstract
There are several systemic inflammatory changes accompanying the atherosclerotic arterial disease in humans. Anyhow the question whether inflammation is directly involved into the pathogenesis of atherosclerosis of systemic inflammatory markers represent merely generalized response of the human organism to the damage of the vessel wall remains to be solved in the future. Irrespectively of the role of inflammation in the etiopathogenesis of atherosclerosis, the most probable key and starting event in this disease is endothelial damage. Endothelial damage is accompanied by functional changes of the vessel wall and circulatory markers of endothelial dysfunction.
The main aim of our investigation is to detect the role of inflammation in different forms and locations of atherosclerotic disease process, the usefulness of determination of circulatory markers of endothelial dysfunctional changes of peripheral arteries in detecting the earliest atherosclerotic changes of the vessel wall. We will also study the relationship between aforementioned markers of endothelial dysfunction and the progression of athersclerosis. In addition to this, we would like to find out also whether the drugs, which are most frequentaly used for the treatment of atherosclerotic risk factors and prevention of progression of atherosclerosis influence the expected systemic inflammatory changes in subject at high risk of and in patients with manifest/overt atherosclerotic disease. We could expect that the drogs used in secondary prevention of atherosclerosis will influence systemic markers of inflammation and will favor the hypothesis of involvment of inflammation in atherogenesis. Such a finding will stimulate a search for new, possibly even more active drugs for prevention of inflammation of the vessel wall that probably is the most important cause of cardiovascular event.
