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Inflammation drives atherosclerosis
Atherosclerosis and its clinical complications such as myocardial infarction and stroke represent the leading causes of death in developed countries and are on the rise in the rest of the world. Over the past decades the understanding of the pathomechanisms underlying atherogenesis has been revolutionized. While formerly considered a mere lipid storage disease, extensive basic and clinical data led to the appreciation of inflammation as the key initiator of atherosclerotic lesion formation.
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| Aortic arch | Aortic root | Abdominal aorta |
According to the current “response-to-injury” model, the initiation of atherogenesis involves activation of the endothelium by certain lipid formulations, cytokines, shear stress, and other stressors resulting in expression of adhesion molecules and chemokines. Circulating inflammatory cells such as monocytes and T-cells adhere to the activated endothelium and migrate into the nascent lesions. Upon uptake of modified lipids inflammatory cells produce a plethora of pro-inflammatory cytokines within the plaque leading to a discontinuous plaque growth and clinical symptoms of ischemia. Ultimately, these inflammatory processes may alter the extracellular matrix metabolism by inhibiting collagen synthesis and promotion of collagen break down, rendering the fibrous cap of a plaque weak and prone to rupture. Plaque rupture in the arteries of the heart commonly results in abrupt vessel occlusion leading to the clinical condition known as myocardialinfaction.
Our group shares a profound interest for the inflammatory mechanisms that orchestrate this pro-atherogenic scenario. Particularly we are determined to elucidate pivotal signalling pathways of the major pro-atherogenic cytokines such as the members of the Tumor Necrosis Factor (TNF) receptor family. We believe that this strategy will facilitate the development of causal and selective means of therapeutic intervention. Furthermore we explore inflammatory mechanisms linking inflammation and metabolic disease such as diabetes, insulin resistance, and obesity with atherogenesis since metabolic disease represents the most prominent promoter of atherogenesis in our times.
Currently we focus on the following projects:
- The role of TNF receptor-associated factors (TRAFs) in vascular disease
- Descriptive and functional characterization of CD40L-Mac-1 interactions
- CD40L-induced adipose/endothelial dysfunction
- Characterization of novel inflammatory markers in cardiovascular disease
