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Projects / Programmes source: ARIS

Atherosclerosis and inflammation

Research activity

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 
Keywords
atherosclerosis, inflammation, endothelial dysfunction, adhesion molecules
Evaluation (rules)
source: COBISS
Researchers (24)
no. Code Name and surname Research area Role Period No. of publicationsNo. of publications
1.  18392  Meaz Agič    Researcher  2003 - 2004 
2.  21331  Simona Auman    Researcher  2003 - 2004 
3.  18823  Barbara Ažbe    Researcher  2003 - 2004 
4.  02929  Igor Bardorfer  Cardiovascular system  Researcher  2002 - 2004  18 
5.  07630  PhD Aleš Blinc  Cardiovascular system  Researcher  2002 - 2004  501 
6.  17728  Sonja Bogdanovič    Researcher  2003 - 2004 
7.  08799  Matija Cevc  Cardiovascular system  Researcher  2002 - 2004  139 
8.  04756  Alenka Čeč-Laban  Cardiovascular system  Researcher  2002 - 2004 
9.  11685  PhD Zlatko Fras  Cardiovascular system  Researcher  2002 - 2004  798 
10.  14041  PhD Barbara Gužič-Salobir  Cardiovascular system  Researcher  2002 - 2004  162 
11.  21360  PhD Majda Joras  Cardiovascular system  Researcher  2002 - 2004  11 
12.  00365  PhD Irena Keber  Cardiovascular system  Researcher  2002 - 2004  386 
13.  17729  Bojana Koščak    Researcher  2003 - 2004 
14.  14642  PhD Alenka Mavri  Cardiovascular system  Researcher  2002 - 2004  222 
15.  17732  Jana Mravlje    Researcher  2003 - 2004 
16.  17724  Andreja Pavlovič    Researcher  2003 - 2004 
17.  04548  PhD Pavel Poredoš  Cardiovascular system  Head  2002 - 2004  988 
18.  08094  PhD Mirza Šabovič  Cardiovascular system  Researcher  2002 - 2004  424 
19.  17725  Marinka Tehovnik    Researcher  2003 - 2004 
20.  17727  Milena Urbas    Researcher  2003 - 2004 
21.  05888  PhD Nina Vene-Klun  Cardiovascular system  Researcher  2002 - 2004  170 
22.  03392  MSc Viktor Videčnik  Cardiovascular system  Researcher  2002 - 2004  103 
23.  22067  Karmen Zagorc    Researcher  2003 - 2004 
24.  17733  Majda Zavec    Researcher  2003 - 2004 
Organisations (1)
no. Code Research organisation City Registration number No. of publicationsNo. of publications
1.  0312  University Medical Centre Ljubljana  Ljubljana  5057272000  77,959 
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.
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