Knut Fälker
Knut Fälker Position: Senior Lecturer School/office: School of Medical SciencesEmail: a251dC5mYWxrZXI7b3J1LnNl
Phone: +46 19 301254
Room: X2220
About Knut Fälker
Knut Fälker has studied nutritional sciences at the Justus-Liebig-University, Giessen, Germany. During his studies he became intrigued by the field of pharmacology and performed his Diploma/Master thesis at the Rudolf-Bucheim-Institut for Pharmacology, Medical Faculty, Justus-Liebig-University, Giessen.
Knut defended his doctoral thesis entitled “Activation and regulation of the extracellular signal-regulated kinase 2 (ERK2) in human platelets’, conducted at the Department of Pharmacology and Toxicology, Medical Faculty of the Martin-Luther-University Halle-Wittenberg, Halle an der Saale, Germany, in the year 2005.
Thereafter, he worked as a postdoctoral fellow and researcher in the Disease Group Thrombosis & Angiogenesis, Section Molecular Biology and Biochemistry, at Sanofi-Aventis Deutschland GmbH, Frankfurt am Main, Germany, and the Cardiovascular Inflammation Research Centre (CIRC) at the Faculty of Health Sciences, Linköping University, Sweden.
In 2013, Knut joined Örebro University’s School of Medical Sciences as a researcher affiliated with the Cardiovascular Research Centre (CVRC). At present, Knut is a member of the "Translational Cardiovascular Research Group" at the School of Medical Sciences at Örebro University.
Research and associated assignments
Knut Fälker’s research is focused on understanding the physiology of human platelets (also designated thrombocytes.) Platelets play a pivotal role in physiological haemostasis, which is the human body's instant response to blood vessel injury to stop bleeding.
In contrast, under pathophysiological conditions, such as atherosclerosis and an eventual atherosclerotic plug rupture, inappropriate platelet activation and platelet-plug formation can cause vascular occlusions resulting in myocardial infarctions or stroke, which are, according to the World Health Organization (WHO), until today the worldwide leading causes for death.
Hence, Knut’s research emphasizes on the investigation of diverse platelet receptors and connected signalling pathways involved in, or contribute to, the activation and regulation of human platelets; and how these mechanisms may contribute to both physiological haemostasis as well as to pathologic thrombus formation. Since human platelets, due to their non-nucleated nature, cannot be genetically modified, his main challenge often lies in the development of experimental strategies and the use of pharmacological tools to specifically modulate platelet signalling pathways and functional responses.
As a renowned member of the "platelet community", Knut serves as reviewer for scientific journals, such as Haematologica, Thrombosis & Haemostasis, or FEBS letters, as well as for committees such as the UK research council or the organizers of the European Platelet Meeting.
Teaching and institutional assignments
Knut Fälker is the current course-coordinator and examiner of the third semester of Örebro University's medical program, the latter in which he also serves as an experienced PBL-group tutor and project-supervisor.
Knut is further a steering member of the council for the international Master’s programme Experimental Medicine, as well as examiner in the profile Cardiovascular Biomedicine, the latter in which he is vividly involved as lecturer as well as a supervising tutor for practical trainings and Master’s projects. Further, Knut initiated and substantially developed the programme’s quite unique approach for personally counselling and supporting students in their professional development and networking.
For the School of Medical Sciences’ open seminar series "MV Science Forum", Knut has been designated as the overall coordinator until spring 2023, where Knut served as representative for the Cardiovascular Research Centre (CVRC), and frequently arranged for highly appreciated talks from national and international speakers.
Medical innovation
Cardiovascular diseases (CVDs) are the leading cause of death globally, taking an estimated 17.9 million lives each year. More than four out of five CVD deaths are due to ischemic events such as myocardial infarction and stroke (source WHO).
Patients experiencing a myocardial infarction or stroke reaching the emergency department are immediately set under a regime of dual antiplatelet therapy (DAPT) to hinder the progression of vascular occlusion. Patients surviving such an event will receive long-term if not lifelong DAPT.
While preventing ischemic recurrences, inhibition of platelet function by DAPT is clearly associated with an increased bleeding risk, a feared complication during surgery leading to significant morbidity and mortality.
Today, there are no haemostatic patches on the market which effectively can stop bleedings in patients under DAPT undergoing acute surgery.
Neericor AB is developing novel haemostatic patches to stop and avoid bleeding complications in patients under DAPT during acute (cardio)vascular surgery. Industrial Partners in this pursuit are Marinova pty ltd, Tasmania, Australia, and Collagen Solutions plc, Minnesota, USA.
In 2022, Neericor AB has been launched as one of Örebro University’s spin-out companies by Knut Fälker and Magnus Grenegård, School of Medical Sciences, Örebro University, Peter Påhlsson, Department of Biomedical and Clinical Sciences, Linköping University, and Mats Dreifaldt, Department of Cardiothoracic and Vascular Surgery, Örebro University Hospital; strongly supported by Örebro University’s Innovation Office. The Örebro University Holding AB is one of the main shareholders. Neericor AB has patents pending for the EU and USA.
Neericor AB appreciates funding and support from Vinnova through verification funding (VFT & VFT+), Inkubera, and Almi, as well as from the Örebro University Holding AB.
Research projects
Active projects
Publications
Articles in journals
- Ljungberg, L. , Zegeye, M. M. , Kardeby, C. , Fälker, K. , Repsilber, D. & Sirsjö, A. (2020). Global Transcriptional Profiling Reveals Novel Autocrine Functions of Interleukin 6 in Human Vascular Endothelial Cells. Mediators of Inflammation, 2020. [BibTeX]
- Fälker, K. , Ljungberg, L. , Kardeby, C. , Lindkvist, M. , Sirsjö, A. & Grenegård, M. (2019). Adrenoceptor α2A signalling countervails the taming effects of synchronous cyclic nucleotide-elevation on thrombin-induced human platelet activation and aggregation. Cellular Signalling, 59, 96-109. [BibTeX]
- Lindkvist, M. , Fernberg, U. , Ljungberg, L. , Fälker, K. , Fernström, M. , Hurtig-Wennlöf, A. & Grenegård, M. (2019). Individual variations in platelet reactivity towards ADP, epinephrine, collagen and nitric oxide, and the association to arterial function in young, healthy adults. Thrombosis Research, 174, 5-12. [BibTeX]
- Kardeby, C. , Fälker, K. , Haining, E. J. , Criel, M. , Lindkvist, M. , Barroso, R. , Påhlsson, P. , Ljungberg, L. & et al. (2019). Synthetic glycopolymers and natural fucoidans cause human platelet aggregation via PEAR1 and GPIbα. Blood Advances, 3 (3), 275-287. [BibTeX]
- Zegeye, M. M. , Lindkvist, M. , Fälker, K. , Kumawat, A. K. , Paramel Varghese, G. , Grenegård, M. , Sirsjö, A. & Ljungberg, L. U. (2018). Activation of the JAK/STAT3 and PI3K/AKT pathways are crucial for IL-6 trans-signaling-mediated pro-inflammatory response in human vascular endothelial cells. Cell Communication and Signaling, 16 (1). [BibTeX]
- Tengdelius, M. , Kardeby, C. , Fälker, K. , Griffith, M. , Påhlsson, P. , Konradsson, P. & Grenegård, M. (2017). Fucoidan-Mimetic Glycopolymers as Tools for Studying Molecular and Cellular Responses in Human Blood Platelets. Macromolecular Bioscience, 17 (2). [BibTeX]
- Donner, L. , Fälker, K. , Gremer, L. , Klinker, S. , Pagani, G. , Ljungberg, L. U. , Lothmann, K. , Rizzi, F. & et al. (2016). Platelets contribute to amyloid-β aggregation in cerebral vessels through integrin αIIbβ3-induced outside-in signaling and clusterin release. Science Signaling, 9 (429). [BibTeX]
- Fälker, K. , Klarström-Engström, K. , Bengtsson, T. , Lindahl, T. L. & Grenegård, M. (2014). The Toll-like receptor 2/1 (TLR2/1) complex initiates human platelet activation via the src/Syk/LAT/PLC gamma 2 signalling cascade. Cellular Signalling, 26 (2), 279-286. [BibTeX]
- Fälker, K. , Nazare, M. , Wonerow, P. & Kozian, D. H. (2013). Targeting Platelet G Protein-Coupled Receptors for Antithrombotic Therapy. Drug development research (Print), 74 (7), 440-449. [BibTeX]
- Elvers, M. , Grenegård, M. , Khoshjabinzadeh, H. , Münzer, P. , Borst, O. , Tian, H. , Di Paolo, G. , Lang, F. & et al. (2012). A novel role for phospholipase D as an endogenous negative regulator of platelet sensitivity. Cellular Signalling, 24 (9), 1743-52. [BibTeX]
- Osman, A. & Fälker, K. (2011). Characterization of human platelet microRNA by quantitative PCR coupled with an annotation network for predicted target genes. Platelets, 22 (6), 433-41. [BibTeX]
- Fälker, K. , Haglund, L. , Gunnarsson, P. , Nylander, M. , Lindahl, T. L. & Grenegård, M. (2011). Protease-activated receptor 1 (PAR1) signalling desensitization is counteracted via PAR4 signalling in human platelets. Biochemical Journal, 436 (2), 469-480. [BibTeX]
- Fälker, K. , Lange, D. & Presek, P. (2005). P2Y12 ADP receptor-dependent tyrosine phosphorylation of proteins of 27 and 31 kDa in thrombin-stimulated human platelets. Thrombosis and Haemostasis, 93 (5), 880-888. [BibTeX]
- Fälker, K. , Lange, D. & Presek, P. (2004). ADP secretion and subsequent P2Y12 receptor signalling play a crucial role in thrombin-induced ERK2 activation in human platelets. Thrombosis and Haemostasis, 92 (1), 114-23. [BibTeX]
Manuscripts
- Lindkvist, M. , Ljungberg, L. U. , Fälker, K. , Ramström, S. , Kardeby, C. , Sirsjö, A. & Grenegård, M. IL-6 trans-signalling inhibits micro- and macro-aggregation induced by epinephrine in human platelets. [BibTeX]