Emiel van der Vorst
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.