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Cambridge Cardiovascular



Cardiac arrhythmogenesis in murine models

My current interests are in the mechanisms of atrial and ventricular arrhythmia in genetically modified murine models for ion channel and metabolic abnormalities, and explorations for possible therapeutic targets.

My team has focused on understanding the transduction and propagation of biological signaling events at the cellular and systems levels. These include the initiation of striated muscle and osteoclast activity, mechanisms of cardiac arrhythmogenesis and cortical spreading depression in the central nervous system.

We have developed and integrated electrophysiological, spectrofluorimetric, confocal/electronmicroscope, magnetic resonance imaging (MRI), and mathematical modeling methods in genetically modified murine systems. 

Our current translational work on cardiac arrhythmogenesis studies spreading physiological cellular and systems phenomena, including the roles of after-depolarization, 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 models are being used to develop a systematic classification of arrhythmogenic mechanisms in these conditions. The work includes 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, my team is now proceeding to examine arrhythmic events in translational models for common human disorders such as metabolic disease and cardiac failure.


Key publications: 

Most recent publications are available through PubMed.

Sodium channel haploinsufficiency and structural change in ventricular arrhythmogenesis. Jeevaratnam K, Guzadhur L, Goh YM, Grace AA, Huang CL. Acta Physiol (Oxf). 2016 Feb;216(2):186-202.

Flecainide exerts paradoxical effects on sodium currents and atrial arrhythmia in murine RyR2-P2328S hearts. Salvage SC, King JH, Chandrasekharan KH, Jafferji DI, Guzadhur L, Matthews HR, Huang CL, Fraser JA. Acta Physiol (Oxf). 2015 Jul;214(3):361-75.

Computational analysis of the electromechanical consequences of short QT syndrome. Huang CL. Front Physiol. 2015 Feb 11;6:44.

A new look at sodium channel β subunits. Namadurai S, Yereddi NR, Cusdin FS, Huang CL, Chirgadze DY, Jackson AP. Open Biol. 2015 Jan;5(1):140192.

Action potential wavelength restitution predicts alternans and arrhythmia in murine Scn5a(+/-) hearts. Matthews GD, Guzadhur L, Sabir IN, Grace AA, Huang CL. J Physiol. 2013 Sep 1;591(17):4167-88.

SERCA2a stimulation by istaroxime: a novel mechanism of action with translational implications. Huang CL. Br J Pharmacol. 2013 Oct;170(3):486-8.


Professor of Cell Physiology
Professor Christopher  Huang


Person keywords: 
cardiac electrophysiology
Membrane biophysics