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Our goal is to unravel the relationship between metabolic syndrome and cardiovascular diseases. This syndrome clusters obesity, dyslipidemia, diabetes, and hypertension. It is associated with high cardiovascular risk due to high state of inflammation and oxidative stress.
The primary event in atherosclerosis is the loss of endothelial function that is associated with increased adhesion and infiltration of monocytes in the arterial wall. Our primary focus is oxidized LDL that contributes to atherosclerotic plaque progression and plaque rupture.
We use a porcine atherosclerosis model to identify gene correlates of oxidized LDL in circulating monocytes and plaque macrophages.
We use a mouse model of the metabolic syndrome that shows accelerated atherosclerotic lesion progression primarily due to increased oxidative stress resulting from impaired HDL-associated antioxidant defense.
Weight loss in this model is associated with inhibition of atherosclerosis and improvement of heart function due to restored activity of Peroxisome Proliferator Activated Receptors in adipose tissue, vessel wall and heart. Currently we search for genes in circulating monocytes which cause their increased infiltration in the adipose tissue and vessel wall of obese persons. |
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