Atherosclerosis and mitochondrial dysfunction – possible links
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Cardiology Department with Cardiology Intensive Care Unit, Ministry of the Interior and Administration Hospital, Lublin, Poland
Department of Cell and Organism Biology, Lund University, Lund, Sweden; Department of Medical Biology, Institute of Agricultural Medicine, Lublin, Poland
Magdalena Stachura   

Cardiology Department with Cardiology Intensive Care Unit, Ministry of the Interior and Administration Hospital, Grenadierów 3, 20-331 Lublin, Poland.
J Pre Clin Clin Res. 2009;3(2):91–94
Atherosclerosis is one of the most widespread diseases and remains a leading cause of death in developed countries. Traditional risk factors, such as obesity, cigarettes smoking, diabetes, and arterial hypertension, are insufficient for predicting which patients are in the group at highest risk for developing atherosclerosis. Knowledge about low-intensity inflammatory processes in the blood vessels, links between traditional risk factors and the forming of atherosclerotic plaques forming is constantly being extended, resulting in new strategies for treatment. Oxidative stress is described as an imbalance between reactive oxygen species (ROS) production and their elimination, in favour the former, and is believed to be characteristic of diabetes, hypertension and atherosclerosis. Increased level of ROS is considered an important cause of endothelial dysfunction occurring in the above-mentioned diseases by triggering the mitochondrial dysfunction. There is also evidence suggesting a possible link between mitochondrial dysfunction and cardiovascular diseases, thus indicating new directions for the examination of mechanisms of atherosclerosis.
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