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Dr Ewan Fowler
- Available for postgraduate supervision
Teams and roles for Ewan Fowler
Research Fellow
School of Biosciences
Overview
Biography
Ewan Fowler is a British Heart Foundation Intermediate Basic Sciences Research Fellow in the School of Biosciences at Cardiff University. He received his BSc (Hons) from the University of Glasgow in Human Exercise Physiology, then completed an MRes and PhD at the University of Leeds focussed on right ventricular failure resulting from pulmonary arterial hypertension. He then spent 6 years in the laboratory of Prof Mark Cannell at the University of Bristol, where he made important contributions understanding how dysregulated calcium signalling can give rise to arrhythmias. In 2020 he joined Cardiff University and established the Cellular Cardiology Research Group. Work undertaken in this group aims to understand the factors that regulate intracellular calcium normally and can become maladapted in disease, resulting in arrhythmias and sudden death. He is an advocate for Early Career Researchers and co-chairs the BIOSI ECR network and is currently a committee member of the Wales Heart Research Institute.
Research Interests
The central question being addressed by Ewan Fowler’s research group is: how do microscopic fluctuations in intracellular calcium (calcium sparks) in cardiac myocytes impact the rhythm and contractility of the heart? The action potential triggers the near-synchronous activation of ~10,000 calcium sparks, which underlies the calcium transient responsible for heart muscle contraction. On the other hand, spontaneous diastolic calcium sparks occur at much lower levels between beats (~ 1 per second), but are associated with irregular heart rhythm. Current work is focussed on a more recently discovered form of calcium sparks that occur at an intermediate frequency (~100 per second) during the recovery phase of the calcium transient and that are also thought to be a risk factor for arrhythmias. Modulating their behaviour could be a novel therapeutic target. A wide range of cutting-edge physiological techniques are employed to accomplish this, including: super-resolution live cell imaging, patch clamp electrophysiology, calcium/voltage optical mapping in perfused hearts, recombinant protein engineering, and detailed mathematical modelling.
The laboratory has received support from the British Heart Foundation, Royal Society, Heart Research Wales, Wales Heart Research Institute and the Physiological Society
The group have active collaborations with institutions across the UK and Europe and have hosted undergraduate and postgraduate students from the UK and USA. If you would like to discuss possible opportunities to conduct cardiac research in the laboratory then please contact FowlerED@Cardiff.ac.uk
Publication
2025
- Fowler, E. D., Diakite, S. L., Gomez, A. M. and Colman, M. A. 2025. Disruption of ventricular activation by subthreshold delayed afterdepolarizations in RyR2-R420Q catecholaminergic polymorphic ventricular tachycardia. Journal of Molecular and Cellular Cardiology Plus 13, article number: 100466. (10.1016/j.jmccpl.2025.100466)
- Zissimopoulos, S. et al. 2025. Compromised repolarization reserve in a murine model of catecholaminergic polymorphic ventricular tachycardia caused by RyR2-R420Q mutation. Journal of Molecular and Cellular Cardiology 206, pp. 127-140. (10.1016/j.yjmcc.2025.07.014)
2023
- Fowler, E. D., Azarov, J. E. and Brette, F. 2023. Editorial: Stretch and the heart: mechanoelectrical coupling and arrhythmias. Frontiers in Physiology 14, article number: 1278561. (10.3389/fphys.2023.1278561)
2022
- Fowler, E. D. and Zissimopoulos, S. 2022. Molecular, subcellular, and arrhythmogenic mechanisms in genetic RyR2 disease. Biomolecules 12(8), article number: e1030. (10.3390/biom12081030)
- Wang, N., Dries, E., Fowler, E. D., Harmer, S. C., Hancox, J. C. and Cannell, M. B. 2022. Inducing Ito,f and phase 1 repolarization of the cardiac action potential with a Kv4.3/KChIP2.1 bicistronic transgene. Journal of Molecular and Cellular Cardiology 164, pp. 29-41. (10.1016/j.yjmcc.2021.11.004)
2020
- Fowler, E. D., Wang, N., Hezzell, M., Chanoit, G., Hancox, J. C. and Cannell, M. B. 2020. Arrhythmogenic late Ca2+ sparks in failing heart cells and their control by action potential configuration. Proceedings of the National Academy of Sciences 117(5), pp. 2687-2692. (10.1073/pnas.1918649117)
2019
- Fowler, E. D., Hauton, D., Boyle, J., Egginton, S., Steele, D. S. and White, E. 2019. Energy metabolism in the failing right ventricle: Limitations of oxygen delivery and the creatine kinase system. International Journal of Molecular Sciences 20(8), article number: 1805. (10.3390/ijms20081805)
2018
- Fowler, E. D. et al. 2018. Beta1-adrenoceptor antagonist, metoprolol attenuates cardiac myocyte Ca2+ handling dysfunction in rats with pulmonary artery hypertension. Journal of Molecular and Cellular Cardiology 120, pp. 74-83. (10.1016/j.yjmcc.2018.05.015)
- Fowler, E. D., Drinkhill, M. J., Stones, R. and White, E. 2018. Diastolic dysfunction in pulmonary artery hypertension: creatine kinase and the potential therapeutic benefit of beta-blockers. Clinical and Experimental Pharmacology and Physiology 45(4), pp. 384-389. (10.1111/1440-1681.12898)
2017
- Diggle, C. P. et al. 2017. A tubulin alpha 8 mouse knockout model indicates a likely role in spermatogenesis but not in brain development. PLoS ONE 12(4), pp. e0174264. (10.1371/journal.pone.0174264)
2015
- Fowler, E. D. et al. 2015. Decreased creatine kinase is linked to diastolic dysfunction in rats with right heart failure induced by pulmonary artery hypertension. Journal of Molecular and Cellular Cardiology 86, pp. 1-8. (10.1016/j.yjmcc.2015.06.016)
- Natali, A. J., Fowler, E. D., Calaghan, S. C. and White, E. 2015. Voluntary exercise delays heart failure onset in rats with pulmonary artery hypertension. American Journal of Physiology - Heart and Circulatory Physiology 309(3), pp. H421-H424. (10.1152/ajpheart.00262.2015)
2014
- Benoist, D. et al. 2014. Systems approach to the study of stretch and arrhythmias in right ventricular failure induced in rats by monocrotaline. Progress in Biophysics and Molecular Biology 115(2-3), pp. 162-172. (10.1016/j.pbiomolbio.2014.06.008)
Articles
- Fowler, E. D., Diakite, S. L., Gomez, A. M. and Colman, M. A. 2025. Disruption of ventricular activation by subthreshold delayed afterdepolarizations in RyR2-R420Q catecholaminergic polymorphic ventricular tachycardia. Journal of Molecular and Cellular Cardiology Plus 13, article number: 100466. (10.1016/j.jmccpl.2025.100466)
- Zissimopoulos, S. et al. 2025. Compromised repolarization reserve in a murine model of catecholaminergic polymorphic ventricular tachycardia caused by RyR2-R420Q mutation. Journal of Molecular and Cellular Cardiology 206, pp. 127-140. (10.1016/j.yjmcc.2025.07.014)
- Fowler, E. D., Azarov, J. E. and Brette, F. 2023. Editorial: Stretch and the heart: mechanoelectrical coupling and arrhythmias. Frontiers in Physiology 14, article number: 1278561. (10.3389/fphys.2023.1278561)
- Fowler, E. D. and Zissimopoulos, S. 2022. Molecular, subcellular, and arrhythmogenic mechanisms in genetic RyR2 disease. Biomolecules 12(8), article number: e1030. (10.3390/biom12081030)
- Wang, N., Dries, E., Fowler, E. D., Harmer, S. C., Hancox, J. C. and Cannell, M. B. 2022. Inducing Ito,f and phase 1 repolarization of the cardiac action potential with a Kv4.3/KChIP2.1 bicistronic transgene. Journal of Molecular and Cellular Cardiology 164, pp. 29-41. (10.1016/j.yjmcc.2021.11.004)
- Fowler, E. D., Wang, N., Hezzell, M., Chanoit, G., Hancox, J. C. and Cannell, M. B. 2020. Arrhythmogenic late Ca2+ sparks in failing heart cells and their control by action potential configuration. Proceedings of the National Academy of Sciences 117(5), pp. 2687-2692. (10.1073/pnas.1918649117)
- Fowler, E. D., Hauton, D., Boyle, J., Egginton, S., Steele, D. S. and White, E. 2019. Energy metabolism in the failing right ventricle: Limitations of oxygen delivery and the creatine kinase system. International Journal of Molecular Sciences 20(8), article number: 1805. (10.3390/ijms20081805)
- Fowler, E. D. et al. 2018. Beta1-adrenoceptor antagonist, metoprolol attenuates cardiac myocyte Ca2+ handling dysfunction in rats with pulmonary artery hypertension. Journal of Molecular and Cellular Cardiology 120, pp. 74-83. (10.1016/j.yjmcc.2018.05.015)
- Fowler, E. D., Drinkhill, M. J., Stones, R. and White, E. 2018. Diastolic dysfunction in pulmonary artery hypertension: creatine kinase and the potential therapeutic benefit of beta-blockers. Clinical and Experimental Pharmacology and Physiology 45(4), pp. 384-389. (10.1111/1440-1681.12898)
- Diggle, C. P. et al. 2017. A tubulin alpha 8 mouse knockout model indicates a likely role in spermatogenesis but not in brain development. PLoS ONE 12(4), pp. e0174264. (10.1371/journal.pone.0174264)
- Fowler, E. D. et al. 2015. Decreased creatine kinase is linked to diastolic dysfunction in rats with right heart failure induced by pulmonary artery hypertension. Journal of Molecular and Cellular Cardiology 86, pp. 1-8. (10.1016/j.yjmcc.2015.06.016)
- Natali, A. J., Fowler, E. D., Calaghan, S. C. and White, E. 2015. Voluntary exercise delays heart failure onset in rats with pulmonary artery hypertension. American Journal of Physiology - Heart and Circulatory Physiology 309(3), pp. H421-H424. (10.1152/ajpheart.00262.2015)
- Benoist, D. et al. 2014. Systems approach to the study of stretch and arrhythmias in right ventricular failure induced in rats by monocrotaline. Progress in Biophysics and Molecular Biology 115(2-3), pp. 162-172. (10.1016/j.pbiomolbio.2014.06.008)
Research
Heart contraction is controlled by calcium channels (called ryanodine receptors, RYR2) that open and close, allowing calcium levels in heart muscle cells to rise and fall, and the heart to contract and relax. Pathological heart conditions, such as heart failure and an inherited syndrome called CPVT, cause RYR2 to become unstable ("leaky"). Exercise and emotional stress increase Ca2+ leak and can provoke potentially fatal irregular heart rhythm. My work aims to develop new ways to make RYR2 less leaky using recombinant proteins as "model drugs" and establish whether existing drugs could be repurposed for alternate uses.
https://www.cardiff.ac.uk/biosciences/research/projects/heart-disease
Biography
I studied Human Physiology & Sport Science as an undergraduate at the University of Glasgow, followed by an MRes and PhD both in the laboratory of Prof Ed White at the University of Leeds. My work at that time focused on the role of energy systems in the failing right ventricle resulting from pulmonary arterial hypertension. I spent part of my PhD at the VU, Amsterdam, learning to perform intact myocyte stretch and contractility measurements, including physiological workloops (to simulate the in vivo cardiac pressure/volume cycle) in failing heart cells. I was a postdoctoral Research Associate in the lab of Prof Mark Cannell, University of Bristol, where I received much of my training in cardiac Ca2+ signalling and electrophysiology. I am currently funded by a 5-year British Heart Foundation Research Fellowship investigating the link between pathological "late Ca2+ sparks" and arrhythmias.
Committees and reviewing
Reviewing Editor, Frontiers in Physiology
Journal reviewer for a variety of scientific publications
Supervisions
I am always interested in supervising PhDs in the areas of:
- Cardiac pathophysiology
- Calcium imaging
- Electrophysiology
Current supervision
