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Dawood Darbar, MBChB, MD

Chief of Division of Cardiology

Professor of Medicine and Pharmacology

University of Illinois at Chicago



Atrial fibrillation (AF) is associated with significant morbidity and increased mortality. Dr. Darbar and others have used positional cloning, candidate gene and whole exome sequencing (WES) approaches to identify AF-causing mutations in cardiac ion channels, signaling molecules and myocardial structural proteins and uncovered novel underlying mechanisms of AF. However, direct impact of these genetic discoveries to the bedside care of patients with AF has been limited because of incomplete understanding of the cellular mechanisms by which mutations cause AF. This is due in part be due to limitations of non-cardiac cell lines, murine models failing to recapitulate human cellular electrophysiology and our inability to study functioning cardiomyocytes (CMs). Although in vitro electrophysiology is an established technique used by us and others to functionally characterize AF-linked mutations, multiple ion channels contribute to the cardiac atrial action potential and assessment of a single ion channel cannot capture the full spectrum of functional changes associated with AF mutations. Recently, atrial CMs derived from human embryonic stem cells were generated to model pre-clinical testing of atrial-specific antiarrhythmic drugs. However, atrial human induced pluripotent stem cell (hiPSC)-CMs have not been used to model AF-linked mutations and elucidate the underlying cellular mechanisms. One major goal of Dr. Darbar’s laboratory is to develop and validate atrial hiPSC-CMs as a novel platform for modeling the electrophysiologic phenotypes of AF-linked mutations, elucidating the underlying cellular mechanisms and identifying novel mechanism-based therapies, thereby enabling a more ‘personalized’
mechanism-based approach to the treatment of AF.


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