Dr Michael Curtis PhD FBPharmS
Reader in Pharmacology
The Rayne Institute
St Thomas' Hospital
London SE1 7EH
Tel: +44 (0)20 7188 1095
Fax +44 (0)20 7188 3902
Michael Curtis graduated from the University of London in 1979 (BSc in Pharmacology) and obtained his PhD in Pharmacology from the University of British Columbia in 1986. Following a Postdoctoral fellowship at St Thomas' Hospital Medical School (1986-1989), he was appointed Lecturer in Pharmacology at King's College London in 1989. He was promoted to Reader in 1996.
Dr Curtis is a member of the Institute of Learning and Teaching (2002) and a registered practitioner of the Higher Education Academy (2004). He is currently Editor in Chief of the Journal of Pharmacological and Toxicological Methods (2001-), Editor in Chief of Pharmacology Research and Perspectives (2013-), Executive Editor of Pharmacology and Therapeutics (1999-), a Senior Editor (and former Editor and Reviews editor) of the British Journal of Pharmacology (continuous from 1998-2015) and Associate Editor of the Journal of Cardiovascular Pharmacology (1993-), and Current Cardiology Reviews (2004-).
He has served as treasurer of the British Society for Cardiovascular Research since 1998. He is a recipient of the Sandoz prize for research of the British Pharmacological Society (1992), a Learned Society Fellowship of the British Pharmacological Society (2004-) and runner up in the Richard Bing prize of the International Society for Heart Research (1992), and is corresponding author of The Lambeth Conventions II (a guidance document on arrhythmia reserach).
Mechanism of phase 2 infarct related arrhythmogenesis
Michael Curtis obtained two recent grants from the British Heart Foundation to explore the mechanism of ventricular fibrillation occurring during evolution of a myocardial infarct (phase 2 VF). This neglected topic has been difficult to study owing to problems with experimental models. Use of surrogate endpoints (electrophysiology) is isolated Purkinje fibres or cells has in the past provided only limited information. We have been examining the dual role of the autonomic nervous system and the process of retaliatory myocardial inflammation in mediating phase 2 VF, and plan to pursue studies over the next few years. A potential collaboration exists with colleagues interested in mechanisms of inflammatory cell recruitment and activation.
Identification and characterisation of new antiarrhythmic drugs
We have a longstanding interest in antiarrhythmic drug mechanism, particularly in the setting of acute myocardial ischaemia, the setting that in experimental models of ischaemic heart disease is most strongly linked with the occurrence of lethal arrhythmias. Funding for this work comes from the sources of new drugs themselves (the pharmaceutical industry) and, for reasons of confidentiality, details cannot be presented here.
Dr Curtis sets up a heart