A. Zirlik, Freiburg
Atherosclerosis and its clinical complications such as myocardial infarction, heart failure, stroke, and peripheral artery disease – just to name the most important ones – is a top killer world-wide. In the last two decades our understanding of the pathophysiology of this disease has fundamentally changed. While we perceived atherosclerosis as a mere lipid storage disease in the early days, we view this disease as a complex chronic inflammatory disorder today. Most likely triggered by cholesterol and its oxidative modifications the endothelium becomes activated and inflammatory cells attach and migrate into the nascent atherosclerotic lesions. Under the control of a network of cytokines and inflammatory cell subsets these lesions grow discontinuously. Depending on their inflammatory state they develop into less inflamed stable plaques causing the clinical picture of angina. Alternatively, they develop into more inflamed lesions prone to rupture, the anatomical correlate of an acute coronary syndrome such as myocardial infarction.
The DGAF creates a forum for all researches and promotes all research focusing on atherosclerosis all the way from lipid metabolism to immunology. Thereby we contribute to a better understanding of this dreadful disease with the ultimate goal to promote new therapeutic concepts.