Atherosclerosis is a chronic but progressive vasculopathy characterized by subendothelial accumulation of lipids and fibrous constituents in middle sized and large arteries and the major substrate for cardiovascular disease. It becomes clinically manifest only at a late stage, generally through acute cardiovascular syndromes that are caused by rupture of an advanced, vulnerable plaque. Vulnerable plaques are typified by a large lipid core underlying a thin fibrous cap and abundant inflammatory cell deposits in their adventitia and shoulder regions. The Experimental Vascular Pathology group aims to unravel the underlying mechanisms of atherosclerotic plaque development and destabilization, using a combination of in vitro and in vivo approaches, including proteomics, transcriptomics, sophisticated bio-informatic analyses, experimental models, and semi-automated, high-throughput functional screening and imaging tools.
Specific research lines focus on
- Define and reinstruct Macrophage hetereogeneity and function in atherosclerotic plaques (Prof. Dr. E. Biessen)
- Role of the fibroblast, hypoxia, angiogenesis and autophagy in atherosclerosis (Dr. Sluimer)
- Membrane proteases (ADAMs) and their regulation in atherosclerosis (Dr. Donners)
- AMP-activated protein kinase as regulator of tissue homeostasis and therapeutic target (Dr. Neumann)
- Proteomics approaches to identify protein modifications in chronic kidney disease (Prof. Dr. J. Jankowski)
More detailed information on specific research lines can be found with the respective PIs