Dr Rebecca-Ann Burton BSc MSc MBA DPhil FHEA FRSA

Research Overview

My main research interest lies in understanding the underlying causes of arrhythmias, specifically the role for calcium-dysregulation in atrial fibrillation. Calcium ions regulate processes as diverse as cell motility, gene transcription, muscle contraction, exocytosis and numerous proteins are modulated directly/indirectly by calcium. It is becoming increasingly more apparent that alterations in cardiac calcium regulation may be critical in mechanical dysfunction and arrhythmogenesis. To address these questions, funded by the Wellcome Trust and Royal Society in 2015, I moved to set up my own lab in the Department of Pharmacology, University of Oxford. My lab focused on employing state-of-the-art technologies using an interdisciplinary approach to study single cells to cultured atrial tissue to complex, intact tissue models, using high resolution imaging techniques such as electron microscopy, state of the art tissue engineering in order to specifically control calcium signalling and novel microscopy allowing me to image global and sub-cellular events in at high spatio-temporal resolution, furthering our mechanistic understanding with direct relevance to the development of clinical therapies some of these technologies I have created myself. My Sir Henry Dale Project is a truly interdisciplinary project; as such it relies on the collaboration between global groups in several scientific areas.

On going research:
In March 2024 I joined the Department of Pharmacology and Therapeutics. My current research plans build on my training and research experience over the last 20 years involving basic cardiovascular research at the organ, tissue, cellular-levels and translational work in whole animals and patients investigating the causes of arrhythmogenesis of atrial aetiology as well as diseases where sympathetic perturbations have been reported (specifically hypertension and heart failure). I believe that integration of research across levels, combined with direct and multiple level iteration between experimental, theoretical and computational work, is the key to understanding complex physiological systems and pathologies.
The main cause of mortality and morbidity in atrial fibrillation (AF) is inadequate rate or rhythm control with pharmaceutical methods. Anisotropic cellular and subcellular architecture, electrical state, and shape are some of the elements that are necessary to understand the genesis and maintenance of atrial arrhythmias. Studies have indicated that calcium dysregulation plays a significant part in AF. My research employs a multidisciplinary approach, encompassing advanced tissue engineering, optogenetics, conventional electrophysiology, and the creation of novel high-speed optical imaging tools, to enhance our mechanistic knowledge. The findings will contribute to a deeper comprehension of the fundamental biological processes behind sub-cellular calcium signaling and the aetiology of AF, both of which are important for the creation of novel treatment approaches.
Through my graduate studies, postdoctoral research and teaching (Undergraduate and Post-Graduate Lecturing), I have strived to build a foundation in both basic science and translational research, while also developing the ability to cross traditional boundaries between fields of investigation, so that I may pursue an integrative approach, essential in my future career as a scientist striving to improve clinical therapy.