The Chaudhuri lab studies mitochondrial calcium signaling and intracellular ion channels. A main goal is to define how heart failure alters mitochondrial calcium signalling, since calcium is a potent stimulator of ATP synthesis. A second goal is to study intracellular ion channels, utilizing our extensive experience in subcellular electrophysiological analysis.
The Computational Electrocardiology Lab (CEG) studies electrocardiographic mapping of the heart and body surface. Specific research areas includes cardiac electrophysiology in the study of acute ischemia and repolarization abnormalities; and computational electrophysiology in solving electrocardiographic forward and inverse problems.
The Drakos Lab studies myocardial recovery in the chronic heart failure (HF) setting and the acute setting (i.e. acute HF/cardiogenic shock). Several ongoing research projects are focused on understanding the clinical, metabolic and molecular profile of the failing and recovered heart and utilize biological information derived from studies in humans, small and large animal HF models to help understand, predict and manipulate myocardial recovery.
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 Franklin lab studies how the packaging of DNA around nucleosomes influences specific patterns of gene expression and how this packaging is modulated during disease to alter transcriptional activity. Their research aims to understand the mechanistic basis for how remodeling of chromatin induces the re-expression of fetal genes in the heart during the development of hypertrophy and failure.
The Hoareau laboratory focuses on acute care translational research. Specifically, we study novel therapeutic approaches to mitigate ischemia-reperfusion injury in hemorrhagic shock. We work toward preserving mitochondrial function, the essential cell machinery for energy production. We seek to accelerate the transition of new therapies to clinical practice
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 Palatinus Laboratory focus is on targeting this trafficking defect to rescue the cardiomyopathy and sudden death observed in a mouse model of arrhythmogenic cardiomyopathy with the eventual goal to bring these therapeutic strategies to the bedside for preventing sudden cardiac death and treating cardiac arrythmias.
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 Sachse lab studies structure and function of tissues, cells, and proteins of the normal, diseased, and aged heart. Specific research areas are cardiac remodeling in disease, with age and after therapy, intraoperative microscopy and spectroscopy, and computer modeling of fibrotic tissues.
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.