Research interests

Inflammation of both the endothelium and circulating immune cells play an important role in the progression of atherosclerosis. In the last years it has been shown that alterations in the intracellular metabolism of immune cells, more specifically monocytes, is the driving force behind their inflammatory phenotype. This is important, since mapping this lipid and lipoprotein-induced metabolic reprogramming paves the way for future therapeutic strategies to target and or reverse this metabolic phenotype in order to slow down atherosclerosis. 

However, research in the context of vascular metabolism, i.e. the role of metabolic alterations in steering blood vessel inflammation, is still in its infancy. In this line of research we aim to investigate the role of endothelial cell metabolism in driving cardiovascular disease, in order to gain new insight in the crosstalk between this metabolism-driven inflammatory response of the endothelium under hyperlipidemic conditions. In addition, we have a strong focus on optimization of treatment of athero-thrombotic cardiometabolic diseases by performing preclinical pathophysiological research.


Vascular and Valve Inflammatory and metabolic responses

Research output

  1. Atherogenic Lipoprotein(a) Increases Vascular Glycolysis, Thereby Facilitating Inflammation and Leukocyte Extravasation

    Research output: Contribution to journalArticleAcademicpeer-review

  2. Inhibition of PFKFB3 Hampers the Progression of Atherosclerosis and Promotes Plaque Stability

    Research output: Contribution to journalArticleAcademicpeer-review

  3. Metabolism: The road to inflammation and atherosclerosis

    Research output: Contribution to journalArticleAcademicpeer-review

  4. Remnant Cholesterol Elicits Arterial Wall Inflammation and a Multilevel Cellular Immune Response in Humans

    Research output: Contribution to journalArticleAcademicpeer-review

View all (65) »

ID: 67966