Program Leaders
Young ACS
Research Theme
Atherosclerosis is a progressive disease characterized by the accumulation of lipids, inflammatory cells, and fibrous elements within the arterial walls, leading to the formation of plaques. These plaques can narrow the arterial lumen, reducing blood flow, and may rupture, causing thrombotic events. Over time, the atherosclerotic process contributes to major cardiovascular complications such as myocardial infarction, stroke, and peripheral arterial disease. The development of atherosclerotic plaques is driven by a complex interplay of vascular cell types and molecular signals. Endothelial cells, which line the arteries, play a crucial role in maintaining vascular homeostasis. Endothelial dysfunction is associated with risk factors such as hypertension, smoking, dyslipidemia, and diabetes, which are influenced by lifestyle and genetic background. The onset of atherosclerosis is characterized by increased vascular permeability and the recruitment of monocytes and macrophages. These immune cells engulf lipids to become foam cells, a hallmark of early plaque development. Smooth muscle cells residing in the vessel wall contribute to atherosclerotic plaque formation by expanding and adopting foam cell, fibrotic, or calcifying phenotypes. T-lymphocytes and other immune cells release pro-inflammatory cytokines that exacerbate plaque progression and destabilization.
Aortic diseases such as aortic aneurysms (abnormal dilations) and aortic dissections (tears in the vessel wall) are life-threatening conditions. Aortic dissections involve an acute tear in the aortic intima that allows blood to enter the vessel wall, creating a false lumen that can obstruct blood flow to vital organs. Development of aortic disease is multifactorial and complex to investigate. Atherosclerosis and aortic diseases share many pathophysiological features: vascular matrix remodeling, smooth muscle cell dysfunction, and chronic inflammation lead to degradation of the aortic wall’s structural integrity, making it prone to dissection or rupture. Furthermore, the same risk factors that drive atherosclerosis, such as hypertension, smoking, and lifestyle factors, along with genetic predispositions, can also contribute to the development and progression of aortic disease.
Understanding the pathophysiological processes underlying atherosclerosis and aortic disease is crucial for developing strategies to prevent, detect, and manage these conditions. Advances in imaging techniques, medical therapies, and surgical interventions have improved outcomes for patients, but continued research and public health efforts are essential to reduce the global burden of atherosclerotic and aortic disease.
Research strategy
Building on these insights, our research at Amsterdam UMC adopts a multidisciplinary approach that integrates molecular biology, pre-clinical model systems, genetics, imaging, and clinical studies to advance the understanding and management of these diseases. We align diverse research efforts in ageing, lipid metabolism, vascular barrier integrity, inflammation, adiposity, ischemia-reperfusion, arteriogenesis, novel imaging, circulating biomarkers, and clinical translation. Our research lines focus on healthy aging, prevention of complications and cardiovascular diseases with a personalized approach. We conduct studies that touch base with digitalization: implementing communication apps, biobanking, data platforms, AI and cover diversity (age, gender and ethnicity). The integrated and collaborative nature of our fundamental, translational and clinical scientists promises a significant impact in this area of research. Through collaboration and innovation, the atherosclerosis and aortic diseases research theme is shaping the future of cardiovascular care, ensuring healthier aging and reducing disease burden for diverse populations worldwide.