Research Labs

The Dosdall lab utilizes cardiac mapping techniques to investigate the onset, maintenance, and treatments for cardiac arrhythmias. Specific areas of emphasis include understanding the mechanisms of irregular arrhythmias such as atrial and ventricular fibrillation and developing improved translational therapies for avoiding and terminating them

The Hong laboratory studies the regulation and remodeling of membrane microdomains of cardiomyocytes during heart failure progression. They study how cardiomyocyte surface microdomains are organized to concentrate ion channels and signaling proteins for proper function and regulation in normal and failing hearts. The research includes the mechanisms of scaffolding protein and cytoskeleton-based maintenance of membrane structures and subdomains important in calcium signaling, turnover mechanisms of microdomains, and the mechanisms of heart failure progression. The Hong lab’s goal is to identify, at the bench, new molecular and cellular targets that can be translated to develop new therapeutic tools for clinical management of heart failure.

The Ranjan lab studies the pathogenesis of cardiac arrhythmias like atrial fibrillation. The research involves using non-invasive imaging like MRI to quantify the structural changes in the atrial myocardium and study its clinical implications. The lab is also keenly interested in developing an imaging modality to confirm the delivery of ablation lesions in real-time in the myocardial tissue.

The Shaw lab asks the question how membrane proteins such as ion channels arrive with specificity to their appropriate subdomain on the sarcolemmal membrane. Proteins cloned during basic investigations also have translational significance in diagnosing and treating failing hearts and organs subjected to ischemic damage.

The Tristani-Firouzi lab studies the structural basis of K+ channel function and the cellular mechanisms that underlie susceptibility to arrhythmia. Specifically, the lab is focused on understanding how voltage-gated K+ channels “sense” the surrounding membrane potential and the mechanism(s) through which voltage-sensing is coupled to channel opening and inactivation.