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Our research mainly seeks to unravel the complexities of cardiac electrical function and its signalling regulation both in physiological and pathological conditions. It will lead to a better mechanistic understanding of hypertrophic and arrhythmic disorders, culminating in the development of more effective therapeutic interventions. We employ cutting-edge techniques encompassing genetic manipulation technologies and multi-scale electrophysiological, optogenetic, and molecular approaches.

Transmission electron microscopy (TEM) imaging: high electron density vesicles (arrowed) typical of catecholamine-containing chromaffin cells detected in cardiac myocytes

My group has made fundamental contributions towards identification of the novel roles of a multifunctional enzyme-p21 activated kinase (Pak1) in the heart. We demonstrated that Pak1 is central to the regulation of cardiac excitation and is a critical signalling hub in cardioprotection. We also have   established Pak1 as a novel therapeutic target for treating cardiac disease conditions including cardiac arrhythmias.

We are now working on the future treatment of heart diseases using Pak1 as a novel target.  Using structure-based rational drug design, we have already developed a series of novel Pak1 activator compounds as starting point compounds for the future drug development for the cardiac conditions.

We recently unveiled a remarkable previously unrecognised population of cardiomyocytes named "Dbh+ Catecholaminergic Cardiomyocytes" (Dbh+ Cate-CMs), paving the way for a potentially groundbreaking advancement in the field of neurocardiology. These cells, which express the enzyme dopamine-beta-hydroxylase (Dbh) and so can synthesise norepinephrine, originate from cardiomyocyte lineage, contribute to the development, maturation, and function of the cardiac conduction system (CCS). More importantly, the findings also suggest a close structural relationship between these cells and sympathetic innervation during the formation of the CCS. The physical co-localization of these cells, primarily within the ventricles, strongly implies a dynamic and vital interaction between Dbh+ Cate-CMs and the autonomic nervous innervation, which is already known to be highly abundant in the CCS. 

Our team

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