A first line of 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 apoptosis, necrosis, autophagy 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.
Overall, 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.
In a second line of research, we study the physiology of the heart, in particular the role of intercellular communication in the heart muscle as an autoregulatory system of heart muscle performance. We focus on the communication via the paracrine action of neuregulin-1.
For this purpose, we use animal models, cell culture, analysis of twitch performance of isolated heart muscle, echocardiography, haemodynamic pressure-volume analyses and molecular biological and immunohistochemical techniques. This line of research is also translational and aims to develop new therapies for left ventricle dysfunction and chronic heart failure.