Imperial College London

DrAliciaD'Souza

Faculty of MedicineNational Heart & Lung Institute

Reader in Cardiac Electrophysiology
 
 
 
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Contact

 

a.dsouza

 
 
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Location

 

Sir Alexander Fleming BuildingSouth Kensington Campus

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Summary

 

Summary

Alicia D’Souza is a cardiac physiologist and a British Heart Foundation Basic Science Intermediate Research Fellow. Alicia’s research group investigates the mechanisms by which ion channels within the heart’s conduction system are controlled in health and in disease. Her interest in this topic began in PhD studies conducted on the physiology of the diabetic heart under the supervision of Professor Jaipaul Singh at the University of Central Lancashire (2012). Alicia then moved to the University of Manchester (2012) to investigate pacemaking in endurance athletes with Professor Mark Boyett. With British Heart Foundation support Alicia began her independent laboratory in 2019, and in 2023 she moved to the Myocardial Function Section of the National Heart and Lung Institute at Imperial College London to take up a Readership in Cardiac Electrophysiology.

Alicia’s team adopts an integrative approach, combining whole organism, tissue, and single cell electrophysiology with multi-omics technologies to investigate the basis of ion channel plasticity. The team is currently investigating molecular therapies for conduction system disease in endurance training, ageing and in heart failure as well new targets to prevent the time-of-day preponderance of certain arrhythmias. Alicia’s work on conduction system dysfunction in athletes and on the circadian control of ion channels has been popularised in the media and led to numerous awards including the International Society for Heart Research/SERVIER Fellowship Prize, the (inaugural) Cairn Research ‘New and Notable’ Prize Lecture and The Physiological Society’s (inaugural) R Jean Banister Prize Lecture. Alicia’s group is also part of a Fondation Leducq Transatlantic Network of Excellence focused on novel pharmacotherapies for sinus node dysfunction.