Emiel van der Vorst

Post doc

Dr Emiel van der Vorst studied Cardiovascular Biology and Medicine at Maastricht University. After an internship in Sydney, Australia in the lab of Prof. Rye and Prof. Barter, he graduated in 2010. In 2015, he obtained his PhD, under the supervision of Prof. Biessen, Prof. De Winther and Dr Donners at the Department of Pathology, CARIM, Maastricht. The title of his thesis was: 'Modulation of vascular inflammation – cell-type specific effects of ADAMs and HDL'.

During his post-doctoral period (2015-2019) at the Institute for Cardiovascular Prevention in the lab of Prof. Weber and Dr Döring, he obtained several personal grants (Humboldt Foundation, FöFoLe, DZHK) to start establishing his own research line. In 2019, he obtained several prestigious personal grants (Veni, IZKF research group grant, Else-Kröner Fresenius), enabling him to start his own group at CARIM and IMCAR (Aachen, Germany). As principle investigator of the Immune-Lipid Crosstalk Research Group, he currently supervises 1 post-doctoral fellow and 3 PhD students.

Dr Van der Vorst focusses on the interplay between lipids and the immune-system in the context of cardiovascular disease (CVD). Recently, evidence is mounting, including from his own research that main driving factors of CVD, dyslipidemia and inflammation, are interdependent and that considerable crosstalk exists between these two. Combining his expertise on high-density lipoproteins (HDL) and chemokine receptors, he will investigate the interplay between these two factors. In addition, the interplay of various other lipids and lipid derivatives with key immunological factors will be investigated, hopefully elucidating new therapeutic targets.

Special interest of his research group also goes to a so far fairly neglected subgroup of patients in respect to cardiovascular risk, being chronic kidney disease (CKD) patients. It has been clearly shown that CKD patients have a severely increased incidence of CVD, clearly demonstrated by the fact that almost half of the CKD patients die from CVD rather than from the primary kidney disease. Intriguingly, this increased CVD risk in CKD patients cannot be fully explained by the classical CVD risk factors like hypertension or dyslipidemia, suggesting the existence of CKD-specific cardiovascular risk factors. The aim is therefore to explore the role of immune-lipid crosstalk as pathological mechanism in CKD that could contribute to this increased CVD-risk.

Department of Pathology
P. Debeyelaan 25, 6229 HX Maastricht 
PO Box 5800, 6202 AZ Maastricht

  • 2024
    • Döring, Y., van der Vorst, E. P. C., Yan, Y., Neideck, C., Blanchet, X., Jansen, Y., Kemmerich, M., Bayasgalan, S., Peters, L. J. F., Hristov, M., Bidzhekov, K., Yin, C., Zhang, X., Leberzammer, J., Li, Y., Park, I., Kral, M., Nitz, K., Parma, L., ... Weber, C. (2024). Identification of a non-canonical chemokine-receptor pathway suppressing regulatory T cells to drive atherosclerosis. Nature cardiovascular research, 3(2), 221-242. https://doi.org/10.1038/s44161-023-00413-9
    • Christ, A., Maas, S. L., Jin, H., Lu, C., Legein, B., Wijnands, E., Temmerman, L., Otten, J., Isaacs, A., Zenke, M., Stoll, M., Biessen, E. A. L., & van der Vorst, E. P. C. (2024). In situ lipid-loading activates peripheral dendritic cell subsets characterized by cellular ROS accumulation but compromises their capacity to prime naïve T cells. Free Radical Biology and Medicine, 210, 406-415. https://doi.org/10.1016/j.freeradbiomed.2023.11.044
  • 2023
    • Kral, M., van der Vorst, E. P. C., Surnov, A., Weber, C., & Doering, Y. (2023). ILC2-mediated immune crosstalk in chronic (vascular) inflammation. Frontiers in Immunology, 14, Article 1326440. https://doi.org/10.3389/fimmu.2023.1326440
    • Maas, S., Jin, H., Lu, C., Nagenborg, J., Manca, M., Karel, J., Cavill, R., Sikkink, C., Yu, B., Nadeau, S., Dos Santos, J., Gijbels, M., Mees, B., Smirnov, E., Sluimer, J., Martins, G., Van der Vorst, E., & Biessen, E. (2023). Identification Of A Prdm1-Regulated T-Cell Network Which Controls T-Cell Driven Plaque Inflammation In Human And Mouse Atherosclerosis. Atherosclerosis, 379(S1), S11-S11. https://doi.org/10.1016/j.atherosclerosis.2023.06.914
    • van der Vorst, E. P. C., Maas, S. L., Theodorou, K., Peters, L. J. F., Jin, H., Rademakers, T., Gijbels, M. J., Rousch, M., Jansen, Y., Weber, C., Lehrke, M., Lebherz, C., Yildiz, D., Ludwig, A., Bentzon, J. F., Biessen, E. A. L., & Donners, M. M. P. C. (2023). Endothelial ADAM10 controls cellular response to oxLDL and its deficiency exacerbates atherosclerosis with intraplaque hemorrhage and neovascularization in mice. Frontiers in Cardiovascular Medicine, 10(1), Article 974918. https://doi.org/10.3389/fcvm.2023.974918
  • 2022
    • Wollenhaupt, J., Frisch, J., Harlacher, E., Wong, D. W. L., Jin, H., Schulte, C., Vondenhoff, S., Moellmann, J., Klinkhammer, B. M., Zhang, L., Baleanu-Curaj, A., Liehn, E. A., Speer, T., Kazakov, A., Werner, C., van der Vorst, E. P. C., Selejan, S.-R., Hohl, M., Böhm, M., ... Noels, H. (2022). Pro-oxidative priming but maintained cardiac function in a broad spectrum of murine models of chronic kidney disease. Redox Biology, 56, Article 102459. https://doi.org/10.1016/j.redox.2022.102459
    • Heuschkel, M. A., Babler, A., Heyn, J., van der Vorst, E. P. C., Steenman, M., Gesper, M., Kappel, B. A., Magne, D., Gouëffic, Y., Kramann, R., Jahnen-Dechent, W., Marx, N., Quillard, T., & Goettsch, C. (2022). Distinct role of mitochondrial function and protein kinase C in intimal and medial calcification in vitro. Frontiers in Cardiovascular Medicine, 9, Article 959457. https://doi.org/10.3389/fcvm.2022.959457
    • van der Vorst, E. P. C., & Lecour, S. (2022). Finding the culprit for the failure of the immune clock as time goes by. Cardiovascular Research, 118(13), e88-e90. https://doi.org/10.1093/cvr/cvac146