Dr
Rebecca-Ann BurtonProfile page
Senior Lecturer and Year 1 Deputy Director in the School of Medicine
Pharmacology & Therapeutics
- Senior Lecturer and Year 1 Deputy Director in the School of MedicinePharmacology & Therapeutics
ABOUT
Personal Statement
As a physiologist and pharmacologist, my research uses bioengineering, advanced imaging, and computational approaches to investigate the mechanisms and consequences of cardiac arrhythmias. I hold an undergraduate degree in Chemistry, Biology and Microbiology and an MSc in Pharmacology and Biotechnology. Following positions with Professors Peter Kohl and Denis Noble at the University of Oxford, I completed a DPhil in Physiology, Anatomy and Genetics (2010) as an Oxford Overseas Research Scholar and, concurrently, an MBA with Merit from Oxford Brookes University. My graduate research was focussed on developing accurate whole heart, structure-function 3D models of the heart to aide pharmacological assessment of drugs and arrhythmias. The experimental data from my doctoral work has been used to develop and validate cardiac modelling by researchers internationally and has been extensively published, sited. My post-doctoral research at the University of Oxford with Professors Gil Bub, Neil Herring and David Paterson, involved developing novel technologies to study the cardiac-neural axis and arrhythmias using high speed imaging techniques and proteomics Nature Photonics. From 2012, I led a pre-clinical study involving Hydroxychloroquine (HCQ). Our research has shown that HCQ can block the pacemaking “funny current” in cardiac sino-atrial nodal cells, funded externally by Oxford Innovation, UK (highly competitive funding). Heart Rhythm 2015
In 2015, I was awarded a Winston Churchill Fellowship in Science and Engineering, undertaking research with Professor Emilia Entcheva at Stony Brook University, New York, and subsequently received the Winston Churchill Medal. Later that year, I was awarded a Sir Henry Dale Fellowship from the Wellcome Trust and Royal Society, enabling me to establish my independent research group at the University of Oxford. In 2020, I was appointed Associate Professor by Oxford's Medical Sciences Division.
My research spans cardiovascular physiology, biophysics, pharmacology, and computational biology, integrating experimental and theoretical approaches from the cellular to whole-organ level. Early work focused on developing anatomically detailed 3D heart models for investigating arrhythmias and drug safety. Together with national and international collaborators, I have contributed to the development and application of novel imaging and proteomic approaches to investigate cardiac-neural interactions and arrhythmogenesis. iScience
Recently published in Cardiovascular Research, this Royal Society and Wellcome Trust-funded study reveals that lysosomes are important regulators of heart rhythm and atrial function. By uncovering lysosomal signalling pathways that influence cardiac electrical activity, the work provides a new perspective on the regulation of cardiac physiology.Cardiovascular Research Journal
Research Overview
My research focuses on understanding the mechanisms underlying cardiac arrhythmias, particularly the role of calcium signalling and dysregulation in atrial fibrillation (AF). Calcium ions regulate a wide range of cellular processes, including excitation-contraction coupling, gene transcription, cell signalling, and membrane excitability. Increasing evidence suggests that disrupted calcium handling contributes to both electrical and mechanical dysfunction in the heart, playing a central role in arrhythmogenesis.
Supported by a Sir Henry Dale Fellowship from the Wellcome Trust and Royal Society, I established my independent research group in the Department of Pharmacology at the University of Oxford in 2015. My group employed interdisciplinary approaches spanning single cells, engineered cardiac tissues, and intact tissue preparations to investigate the mechanisms driving AF. Using advanced methodologies, including electron microscopy, tissue engineering, high-resolution optical imaging, and novel microscopy platforms, we examined calcium signalling from the cellular to the subcellular level with unprecedented spatial and temporal resolution. Several of these technologies were developed within the laboratory through close collaboration with engineers, physicists, and computational scientists.
The Sir Henry Dale programme brought together an international network of collaborators with expertise in cardiovascular physiology, imaging, bioengineering, and computational biology. Through these partnerships, our research has advanced mechanistic understanding of atrial arrhythmias.
On going research:
I joined the Department of Pharmacology and Therapeutics in March 2024. My research seeks to understand how ageing and disease remodel the heart to promote atrial fibrillation and other cardiac arrhythmias. Combining advanced imaging, electrophysiology, tissue engineering, and computational approaches, I investigate how changes in cellular morphology, fibrosis, intercellular organisation, and calcium signalling contribute to arrhythmogenesis. Working from subcellular mechanisms to whole-organ function, my research bridges basic science and clinical translation, with the aim of developing improved therapeutic strategies and patient outcomes in cardiovascular disease.
Recent work:
Lysosomal signalling pathways influence heart rhythm, and regulate atrial function (accepted in Cardiovascular Research 2026) LINK
Proteomic signatures of mitochondrial dysfunction associated with atrial fibrillation in goats LINK
Protocol for endolysosomal proteomics in goat atrial tissue using a refined density-gradient approach LINK
Activation of IP3R in atrial cardiomyocytes leads to generation of cytosolic cAMP LINK
Compartmentalization proteomics revealed endolysosomal protein network changes in a goat model of atrial fibrillation LINK
Atrial Granules in Atrial Cardiomyocytes as Acidic Calcium Stores LINK
Integrated Transcriptomic Profiling Reveals MAPK14-Related Inflammatory Signalling Associated with Postoperative Atrial Fibrillation LINK
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