Jan Nilsson MD, Professor of Experimental Cardiovascular Research, Lund University
Jan Nilsson is Professor of Experimental Cardiovascular Research at Lund University, Sweden. He received is MD, PhD and specialist training in internal medicine at the Karolinska Institute in Stockholm. He has been associate professor of cell biology and professor of medicine at the Karolinska Institute. Jan Nilsson has been visiting professor of medicine at UCLA, chairman of the Atherosclerosis Working Group of the European Society of Cardiology and dean of the medical school at Lund University. He is a member of the editorial board of Arteriosclerosis, Thrombosis and Vascular Biology, the Swedish Royal Academy of Sciences, deputy chairman of the Swedish Research Council and chairman of the Scientific Board of the Swedish Heart and Lung foundation. His research is focused on the role of inflammation and immunity in atherosclerosis with particular emphasis on the role of lipids.
Multiplex protein analysis of biomarkers in atherosclerosis
Development of atherosclerotic plaque vulnerability involves an accumulation of cytotoxic lipids, an inflammation-driven degradation of the plaque extracellular matrix and a loss of cells with repair function. There is a clinical need for good circulating biomarkers that reflect these processes. While different types of inflammatory biomarkers have been extensively studied biomarkers reflecting cell death as well as extracellular matrix degradation and repair are less well characterized. We have recently shown that activation of apoptotic cell death is associated with a release of soluble death receptors such as Fas and TRAIL receptor 2 that can be measured in plasma. Using the proximity extension assay-based OLINK cardiovascular disease panels we could then demonstrate that subjects with high plasma levels of death receptors have an increased risk of cardiovascular disease. Moreover, an increased risk is also observed in subjects with high levels of the matrix metalloproteinases MMP-7 and -12 as well as in subjects low levels of growth factors for vascular smooth muscle cells and vascular progenitor cells.1, 2 These observations provide clinical support for an important role of vascular injury and repair in the development of cardiovascular disease. Indeed, there is evidence that impaired repair vascular is a key factor in cardiovascular complications to diabetes.3
1. Goncalves I, Bengtsson E, Colhoun HM, Shore AC, Palombo C, Natali A, Edsfeldt A, Duner P, Fredrikson GN, Bjorkbacka H, Ostling G, Aizawa K, Casanova F, Persson M, Gooding K, Strain D, Khan F, Looker HC, Adams F, Belch J, Pinnoli S, Venturi E, Kozakova M, Gan LM, Schnecke V, Nilsson J and Consortium S. Elevated Plasma Levels of MMP-12 Are Associated With Atherosclerotic Burden and Symptomatic Cardiovascular Disease in Subjects With Type 2 Diabetes. Arterioscler Thromb Vasc Biol. 2015;35:1723-31.
2. Wigren M, Rattik S, Hultman K, Bjorkbacka H, Nordin-Fredrikson G, Bengtsson E, Hedblad B, Siegbahn A, Goncalves I and Nilsson J. Decreased levels of stem cell factor in subjects with incident coronary events. J Intern Med. 2016;279:180-91.
3. Edsfeldt A, Goncalves I, Grufman H, Nitulescu M, Duner P, Bengtsson E, Mollet IG, Persson A, Nilsson M, Orho-Melander M, Melander O, Bjorkbacka H and Nilsson J. Impaired fibrous repair: a possible contributor to atherosclerotic plaque vulnerability in patients with type II diabetes. Arterioscler Thromb Vasc Biol. 2014;34:2143-50.