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Guido De Meyer
- Research interest:Our research involves the morphological and haemodynamic changes that occur during the development and rupture of atherosclerotic plaques. Various experimental models have been established in rabbits and in genetically modified mice.Recently, we developed for the first time a model of atherosclerosclerotic plaque rupture in mice with clinical end points such as stroke, myocardial infarction and sudden death. Access to human vascular material allows validation and extrapolation of the data obtained in the animal experiments.Using immunohistochemical and molecular biological techniques, the role of autophagy, apoptosis, necrosis, necroptosis as well as neoangiogenesis in the vulnerability of the atherosclerotic plaque is extensively studied.Functional alterations of endothelial and smooth muscle cells in atherosclerotic blood vessels are investigated in isolated cells, vascular ring segments and with electrophysiological techniques. Pharmacological manipulation of the above measured parameters, including the study of potential plaque stabilizing therapies, is also performed.We also investigate arterial stiffening as a common pathophysiological mechanism in cardiac and kidney failure and brain degeneration.This multidisciplinary approach might result in a better understanding of the various factors involved in the etiopathogenesis and clinical consequences of atherosclerosis and might result in new therapeutic interventions.
- Keywords:ARTERIAL STIFFENING, VASCULAR REACTIVITY, ENDOTHELIAL DYSFUNCTION, APOPTOSIS, VULNERABLE PLAQUE, ATHEROSCLEROSIS, AUTOPHAGY, NECROPTOSIS, Pharmacy and pharmacology
- Disciplines:Cardiac and vascular medicine, Inflammation, Cell death , Biomarker discovery and evaluation, Drug discovery and development, Medicinal products, Pharmaceutics, Pharmacognosy and phytochemistry, Pharmacology, Pharmacotherapy, Toxicology and toxinology, Other pharmaceutical sciences
- Research techniques:Immunohistochemical and molecular biological techniques to study the role of autophagy, apoptosis, necrosis, necroptosis as well as neoangiogenesis in the vulnerability of atherosclerotic plaques.Functional alterations of endothelial and smooth muscle cells in atherosclerotic blood vessels are investigated in isolated cells, vascular ring segments and with electrophysiological techniques.High-frequency ultrasound (Vevo-2100; electrocardiography in mice).
- Users of research expertise:Pharmaceutical industry