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Professor Christopher Huang DM (Oxford), ScD (Cambridge), FRSB

My current interests are directed towards the mechanisms of arrhythmogenesis in genetically modified hearts, studied using biophysical, physiological and molecular biological methods.
Professor Christopher Huang, DM (Oxford), ScD (Cambridge), FRSB

Professor of Cell Physiology

Christopher Huang is accepting applications for PhD students.

Office Phone: +44 (0) 1223 333822, Fax: +44 (0) 1223 333840


Chris Huang was awarded a Florence Heale Scholarship to read Medicine and Physiology at The Queen's College, Oxford and completed his preregistration clinical appointments in the Nuffield Department of Medicine, The John Radcliffe Hospital, Oxford. He joined Gonville and Caius College as an MRC Scholar to complete a PhD in membrane biophysics, and then successively became an Assistant Lecturer and Lecturer in Physiology, Reader and finally the Professor of Cell Physiology at Cambridge, whilst being Fellow and Director of Medical Studies at Murray Edwards College. He is also independent nonexecutive director of Hutchison China Meditech and Hutchison Biofilm Solutions, and Manager of the Prince Philip Scholarship fund.

Chris Huang received the LEPRA Award (British Leprosy Relief Association), the Benefactor's (Queen's, Oxford) and Brian Johnson Prizes (Oxford Medical School), as well as the Rolleston (Oxford) and Gedge Prizes (Cambridge) for physiological research. He is/has been editor of the Journal of Physiology, the Monographs of the Physiological Society, Biological Reviews, BMC Physiology and Europace, and has been visiting professor to the Universities of Debrecen (Hungary) and Hong Kong, and Mount Sinai Medical School, New York, Adjunct Professor in Cardiology to Xi’an Jiaotong University (China) and President of the Cambridge Philosophical Society..


Research Interests

Christopher Huang has contributed to understanding of the transduction and propagation of biological signaling events at the cellular and systems levels. This includes the initiation of striated muscle and osteoclast activity, mechanisms of cardiac arrhythmogenesis and cortical spreading depression in the central nervous system. This involved developing and integrating electrophysiological, spectrofluorimetric, confocal/electronmicroscope, magnetic resonance imaging (MRI), and mathematical modeling methods latterly in genetically modified murine systems. His current translational work on cardiac arrhythmogenesis similarly studies spreading physiological cellular and systems phenomena. It has separated the roles of after-depolarization phenomena, conduction velocity, restitution gradients, refractoriness and altered intracellular Ca2+homeostasis in ventricular arrhythmogenesis in hypokalaemic and genetically modified murine cardiac models for the Brugada, LQT3, LQT5, Scn3b-/-, catecholaminergic polymorphic ventricular tachycardic and metabolic syndromes. These arrhythmic exemplars are being used to develop a systematic classification of arrhythmogenic mechanisms in these conditions. It is separating the roles of after-depolarization and refractory phenomena, restitution gradients and altered intracellular Ca2+ homeostasis and conduction velocity in initiation of ventricular arrhythmogenesis potentially leading to sudden cardiac death. Having characterized fundamental arrhythmic mechanisms in experimental platforms recapitulating specific ion channel disorders, He is now proceeding to examine arrhythmic events in translational models for common human disorders such as metabolic disease and cardiac failure.


Part Ia Physiology: Physiology of muscle

Part II Physiology: Cellular physiology. Advanced electrophysiology classes in  microelectrode recording, cable analysis and loose patch clamping.

Professorial Fellow and Director of Medical Studies, Murray Edwards College.


I have also written the following textbooks:

Glasby, M.A. & Huang, C.L-H. (Eds).  (1995). Applied Physiology for Surgery and Critical Care.  Butterworth-Heinneman. 756pp.

Zaidi, M., Adebanjo, O. A. & Huang, C. L-H. (1998). (Eds.).  Molecular and cellular biology of bone. In: E. E. Bittar (Ed.): Advances in Organ Biology. Vols. 5A, B & C. (926 pp). JAI Press: Stanford, CT. & London. 

Usher-Smith, J. A., Murrell, G.A.C., Ellis, H.E. & Huang, C.L.-H. (2010). Research in Medicine: Planning a project – writing a thesis. 3/e. (2/e 1999) (1/e: 1990). Cambridge University Press.

Keynes, R. D., Aidley. D. J. & Huang, C. L-H. (2011). Nerve and Muscle 4/e. Cambridge University Press. ISBN: 9780521519557]

Chambers, D., Huang, C. L-H & Matthews, G.D.K. (2014). Basic Physiology for Anaesthetists. Cambridge University Press.


Key Publications

Wang Y, Tsu, H, Ke Y, Si Y, Li Y, Davies L, Cartwright EJ, Venetucci L, Terrar DA,  Zhang H, Huang CL-H, Solaro RJ, Wang,Lei M, (2014), Pak1 is required to maintain ventricular Ca2+ homeostasis and electrophysiological stability through SERCA2a regulation in mice, Circulation Arrhythmia, 7:938-948 PMID: 25217043

Zhang Y, Guzadhur L, Jeevaratnam K, Salvage SC, Matthews GDKM, Lammers WJ, Lei M, Huang CL-H, Fraser JA, (2014), Arrhythmic substrate, slowed propagation and increased dispersion in conduction direction in the right ventricular outflow tract of murine Scn5a+/- hearts, Acta Physiologica, 211, 559–573 PMID: 24913289

Matthews GDK, Guzadhur L, Sabir IN, Grace AA, Huang CL-H, (2013), Action potential wavelength restitution predicts alternans and arrhythmia in murine Scn5a+/- hearts, Journal of Physiology, 591, 4167-4188 PMID: 23836691

King JH, Wickramarachchi C, Kua K, Du Y, Jeevaratnam K, Matthews HR, Grace AA, Huang CL-H, Fraser JA, (2013), Loss of Nav1.5 expression and function in murine atria containing the RyR2-P2328S gain-of-function mutation, Cardiovascular Research, 99, 751-759  CVR-2013-82R2 PMID: 23723061

Martin CA, Siedlecka U, Kemmerich K, Lawrence J, Cartledge J, Guzadhur L, Brice N, Grace AA, Schwiening C, Terracciano CM, Huang CL-H, (2012), Reduced Na+ and higher K+ channel expression and function contribute to right ventricular origin of arrhythmias in Scn5a+/- mice, Open biology, 2,120072 PMID: 22773948

Wu J, Zhang Y, Zhang X, Cheng L, Lammers W, Grace A, Fraser JA, Zhang H, HuangCL-H, Lei M, (2012), Altered sino-atrial node function and intra-atrial conduction in murine gain-of-function Scn5a+/kpq hearts suggest an overlap syndrome, American Journal of Physiology. Heart, C302, H1510-1523 PMID: 22287583

Matthews GDK, Guzadhur L, Grace AA, Huang CL-H, (2012), Nonlinearity between action potential alternans and restitution which both predict ventricular arrhythmic properties in Scn5a+/-and wild-type murine hearts, Journal of Applied Physiology, 112(11):1847-63 PMID: 22461438

Gurung IS, Medina-Gomez G, Kis A, Baker M, Velagapudi V, Neogi SG, Campbell M, Rodriguez-Cuenca S, Lelliott C, McFarlane I, Oresic M, Grace AA, Vidal-Puig, A, Huang CL-H, (2011), Deletion of the metabolic transcriptional coactivator PGC1β induces cardiac arrhythmia, Cardiovascular Research, 92(1):29-38 PMID: 21632884

Hao X, Zhang Y, Zhang X, Nirmalan M, Davies L, Konstantinou D, Fei T, Dobrzynski H, Wang X, Grace A, Zhang H, Boyett M, Huang CL-H, Lei M, (2011), TGF-β1 mediated fibrosis and ion channel remodeling are key mechanisms producing the sinus node dysfunction associated with SCN5A deficiency and aging, Circulation: Arrhythmia and Electrophysiology, 4:397-406 PMID:21493874

Martin CA, Guzadhur L, Grace AA, Lei M, Huang CL-H, (2011), Mapping of reentrant spontaneous polymorphic ventricular tachycardia in a Scn5a+/- mouse model, American Journal of Physiology. Heart Circ Physiol, 300(5): H1853-1862 #H-00034-2011R2 PMID: 21378142

Martin CA, Grace AA, Huang CL-H, (2011), Spatial and temporal heterogeneities are localized to the right ventricular outflow tract in a heterozygotic Scn5a mouse model, American Journal of Physiology, 300(2):H605-16 (H-00824-2010R1) PMID: 21097662

Zhang Y, Fraser JA, Jeevaratnam K, Hao X, Hothi S, Grace AA, Lei M, Huang CL-H, (2011), Acute atrial arrhythmogenicity and altered Ca2+ homeostasis in murine RyR2-P2328S hearts, Cardiovascular Research, 89(4):794-804 PMID: 20621925

Above: Sodium (Na+) currents in a Brugada Syndrome model. (a) Traces of Na+ currents from myocytes from the left and right ventricles of normal, wild-type and Brugada Syndrome, Scn5a+/- hearts. Traces normalized to cell capacitance. (b) current voltage relationship of Na+ current in myocytes from the four groups. (c) Maximum Na+ current density of each group. (d ) Activation and (e) inactivation curves in myocytes from the four groups, with Boltzmann fits.  Significant differences: asterisks (*), effect of genotype; hashes (#) effect of cardiac ventricle. From: Martin et al, (2012), Open biology, 2,120072.

Above: Re-entry circuit initiation of ventricular arrhythmia in the Brugada Syndrome model. AF:  Right ventricular isochronal propagation maps in a flecainide treated Scn5a+/- heart leading to ventricular tachycardia. G: electrocardiogram (ECG) trace showing a ventricular ectopic initiating polymorphic ventricular tachycardia. Thick black lines denote propagation block. Thin arrows denote lines of propagation. H: part of the same ECG trace, with 8 electrogram traces, at the point of VTinitiation of VT. Electrogram numbers correspond to the channel numbers of the array, as shown in the maps. Each letter corresponds to the corresponding propagation map. A demonstrates crowded isochronal lines in the last sinus beat, area of conduction slowing. A”: repolarization map of the last sinus beat shows increased repolarization heterogeneity in the same area. B. a premature ventricular beat superimposed on this leads to a line of block with impulse propagation flowing around it. C: shows a second VE that results in a reentrant circuit. D: shows the circuit continuing into the next beat to initiate VT. E and F:  the line of block changes, creating a nonstationary vortex, causing a polymorphic arrhythmia (E and F). I: propagation map, ECG, and electrogram traces of the VT propagating as a wave front across the LV from the RV. J: ECG trace of a VE occurring after the T wave.  From: Martin et al, (2012), Open biology, 2,120072.

Above: Conduction properties of isolated sinoatrial node (SAN) preparations. A. Electrograms and activation mapping in young WT and Scn5a+/-, and old WT and Scn5a+/-. B and C. , SAN cycle lengths and sino-atrial conduction times in the four experimental groups. From: Hao et al, Circulation: Arrhythmia and Electrophysiology, 4:397-406. PMID:21493874

Above: Video images from Fluo-3-loaded myocytes showing propagating Ca2+ waves from (a) unstimulated homozygous RyR2-P2328S myocytes studied in the presence of isoproterenol illustrating a propagating increase of local Ca2+ fluorescence running along the cells. (b) in regularly stimulated WT myocyte, the evoked Ca2+ is synchronized over the whole cell surface.