Our current research focuses on vascular biology, inflammation and immune mechanisms and their regulation in atherosclerosis the main underlying cause of cardiovascular diseases (CVD) including lower extremity arterial disease (LEAD). Atherosclerosis is a chronic inflammatory disease of the arteries, which is driven by modified lipids, and continuous recruitment of leukocytes into the activated intima. In the pathophysiology of atherosclerosis, for example chemokines and their receptors orchestrate stage-specific inflammatory recruitment patterns and immune functions of different cell subsets. Hence, we aim at unraveling the role of the chemokine like receptor ChemR23 and the atypical chemokine receptor ACKR3 in chronic vascular inflammation. Moreover,
LEAD has an increasing prevalence due to aging of the human population but is understudied compared to other vascular beds. LEAD risk factors are multiple (genetic factors, traditional risk factors, metabolic and inflammatory factors, socioeconomic factors) with different weighs of association as compared to e.g. coronary artery diseases. Here we aim at understanding mechanisms involved in LEAD-specific atherothrombosis and calcification.
Patients with CVD have a higher risk to develop severe COVID-19 and more likely suffer from long-term effects which are poorly known. To better appreciate the links between CVD and COVID-19, it is important to understand the underlying pathobiology of SARS-CoV-2 infection in vascular cells. Hence, we develop a mouse model of CVD and COVID-19 to unravel long-term effects on vascular health.