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Dr Ewan Fowler
- Ar gael fel goruchwyliwr ôl-raddedig
Timau a rolau for Ewan Fowler
Cymrawd Ymchwil
Ysgol y Biowyddorau
Trosolwyg
Bywgraffiad
Mae Ewan Fowler yn Gymrawd Ymchwil Gwyddorau Sylfaenol Canolradd Sefydliad Prydain y Galon yn Ysgol y Biowyddorau ym Mhrifysgol Caerdydd. Derbyniodd ei BSc (Anrh) o Brifysgol Glasgow mewn Ffisioleg Ymarfer Corff Dynol, yna cwblhaodd MRes a PhD ym Mhrifysgol Leeds yn canolbwyntio ar fethiant fentriglaidd dde o ganlyniad i bwysedd gwaed uchel rhydwelïol yr ysgyfaint. Yna treuliodd 6 blynedd yn labordy'r Athro Mark Cannell ym Mhrifysgol Bryste, lle gwnaeth gyfraniadau pwysig i ddeall sut y gall signalau calsiwm wedi'u camreoleiddio arwain at arrhythmias. Yn 2020 ymunodd â Phrifysgol Caerdydd a sefydlu'r Grŵp Ymchwil Cardioleg Gellog. Nod y gwaith a wnaed yn y grŵp hwn yw deall y ffactorau sy'n rheoleiddio calsiwm mewngellog fel arfer a gall gael ei gamaddasu mewn clefyd, gan arwain at arrhythmias a marwolaeth sydyn. Mae'n eiriolwr dros Ymchwilwyr Gyrfa Gynnar ac yn cyd-gadeirydd rhwydwaith BIOSI ECR ac ar hyn o bryd mae'n aelod o bwyllgor Sefydliad Ymchwil y Galon Cymru.
Diddordebau Ymchwil
Y cwestiwn canolog sy'n cael ei drafod gan grŵp ymchwil Ewan Fowler yw: sut mae amrywiadau microsgopig mewn calsiwm mewngellog (gwreichion calsiwm) mewn myocytau cardiaidd yn effeithio ar rhythm a chontractiledd y galon? Mae'r potensial gweithredu yn sbarduno actifadu bron cydamserol ~ 10,000 o wreichionen calsiwm, sy'n sail i'r transient calsiwm sy'n gyfrifol am gyfangiad cyhyrau'r galon. Ar y llaw arall, mae gwreichion calsiwm diastolig digymell yn digwydd ar lefelau llawer is rhwng curiadau (~ 1 yr eiliad), ond maent yn gysylltiedig â rhythm y galon afreolaidd. Mae'r gwaith cyfredol yn canolbwyntio ar ffurf mwy diweddar o wreichion calsiwm sy'n digwydd ar amledd canolradd (~100 yr eiliad) yn ystod cyfnod adfer y calsiwm dros dro ac y credir hefyd eu bod yn ffactor risg ar gyfer arrhythmias. Gallai modiwleiddio eu hymddygiad fod yn darged therapiwtig newydd. Defnyddir ystod eang o dechnegau ffisiolegol arloesol i gyflawni hyn, gan gynnwys: delweddu celloedd byw uwch-gydraniad, electroffisioleg clamp patch, mapio optegol calsiwm / foltedd mewn calonnau perfused, peirianneg protein ailgyfunol, a modelu mathemategol manwl.
Mae'r labordy wedi derbyn cefnogaeth gan Sefydliad Prydeinig y Galon, y Gymdeithas Frenhinol, Ymchwil y Galon Cymru, Sefydliad Ymchwil y Galon Cymru a'r Gymdeithas Ffisiolegol
Mae gan y grŵp gydweithrediadau gweithredol â sefydliadau ledled y DU ac Ewrop ac wedi croesawu myfyrwyr israddedig ac ôl-raddedig o'r DU ac UDA. Os hoffech drafod cyfleoedd posibl i gynnal ymchwil cardiaidd yn y labordy, cysylltwch â FowlerED@Cardiff.ac.uk
Cyhoeddiad
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)
Ymchwil
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
Bywgraffiad
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.
Pwyllgorau ac adolygu
Reviewing Editor, Frontiers in Physiology
Journal reviewer for a variety of scientific publications
Meysydd goruchwyliaeth
I am always interested in supervising PhDs in the areas of:
- Cardiac pathophysiology
- Calcium imaging
- Electrophysiology
Goruchwyliaeth gyfredol
Gemma Toerien-Howie
Contact Details
+44 29208 74105
Adeilad Syr Martin Evans, Rhodfa'r Amgueddfa, Caerdydd, CF10 3AX