Projects per year
Our laboratory studies the electrophysiology of cardiac muscle and the generation of arrhythmias. Abnormalities in repolarisation, due to disease states or therapeutic drugs, can give rise to arrhythmias. By measuring electrical activity in isolated single cardiac myocytes and in excised perfused intact hearts, we aim to better understand the processes underlying cardiac repolarization and their modulation in disease states. Our projects are currently funded by the British Heart Foundation and Heart Research UK.
Repolarization of the ventricles is associated with the T wave of the electrocardiogram or ECG. The temporal association between repolarization and the T wave in an isolated perfused heart is illustrated below.
I work closely with Drs Jules Hancox in the Cardiovascular Research Laboratories. Currently, I am principal investigator on research projects examining atrial-ventricular differences in ion channels as a basis for atrial-selective antiarrhythmic drug therapy.
Electrical remodelling of the atrium in hypertension
Atrial fibrillation (AF) is the most common disturbance of cardiac rhythm and is associated with significantly increased mortality. Hypertension is the most prevalent independent risk factor for AF. This project using a common model of arterial hypertension is examining changes associated with hypertension in the electrophysiology of the atrium that might contribute to the incidence of AF.
Sex differences in cardiac repolarization
Women are at significantly greater risk than men of the potentially fatal arrhythmia, torsades de pointes. This is associated with sex differences in the processes underlying ventricular repolarization and is likely to involve the sex hormones. This project is examining the roles of the gonadal steroids in sex differences in ventricular repolarization and drug-induced pro-arrhythmia.
G-protein-coupled receptors (GPCR)
Cardiac function is modulated by neurotransmitters and hormones that exert their effects via G-protein-coupled receptors on the membrane surface. In particular, hormones such as endothelin have been associated with pathological changes in cardiac function. A major interest of our group are the mechanisms by which GPCR hormones modulate cardiac cellular electrophysiology.
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- 1 Finished
14/03/16 → 13/03/19
Delayed Ventricular Repolarization and Sodium Channel Current Modification in a Mouse Model of Rett SyndromeCheng, H., Charles, I., James, A. F., Abdala Sheikh, A. P. & Hancox, J. C., 20 May 2022, In: International Journal of Molecular Sciences. 23, 10, p. 1-25 25 p., 5735.
Research output: Contribution to journal › Article (Academic Journal) › peer-reviewOpen AccessFile3 Citations (Scopus)30 Downloads (Pure)
QTc interval and ventricular action potential prolongation in the Mecp2Null/+ murine model of Rett syndromeCheng, H., Charles, I., James, A. F., Abdala, A. P. & Hancox, J. C., 5 Oct 2022, In: Physiological Reports. 10, 19, 12 p., e15437.
Research output: Contribution to journal › Article (Academic Journal) › peer-reviewOpen AccessFile1 Citation (Scopus)14 Downloads (Pure)
Caves, R. E., Carpenter, A., Choisy, S. C. M., Clennell, B., Cheng, H., McNiff, C., Mann, B., Milnes, J. T., Hancox, J. C. & James, A. F., 1 Aug 2020, In: Heart Rhythm O2. 1, 3, p. 206-214 9 p.
Research output: Contribution to journal › Article (Academic Journal) › peer-reviewOpen AccessFile2 Citations (Scopus)59 Downloads (Pure)
Gadeberg, H. C. (Contributor), Bond, R. C. (Contributor), Kong, C. H. T. (Contributor), Chanoit, G. P. (Contributor), Ascione, R. (Contributor), Cannell, M. B. (Contributor) & James, A. F. (Contributor), Dryad, 1 Jun 2017
Data from: Cellular hypertrophy and increased susceptibility to spontaneous calcium-release of rat left atrial myocytes due to elevated afterload
Zhang, H. (Contributor), Cannell, M. B. (Contributor), Kim, S. J. (Contributor), Watson, J. J. (Contributor), Norman, R. (Contributor), Calaghan, S. C. (Contributor), Orchard, C. H. (Contributor), James, A. F. (Contributor), Cannell, M. B. (Contributor) & Orchard, C. H. (Contributor), Dryad, 7 Dec 2016