Professor Christopher Huang

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.