The Cardiac Translational Research Laboratory investigates the biological mechanisms underlying cardiac arrhythmias, inflammatory heart disease and cardiac aging and translates these discoveries into new cardiovascular therapies. Our work integrates fundamental biology with human cardiac cells and tissues, clinically relevant disease models and therapeutic development.
A defining feature of the laboratory is its emphasis on bench-to-bedside translation. Rather than stopping at biological discovery, our programs span the therapeutic-development continuum—from mechanistic studies in human cells and tissues, through small- and large-animal studies, to therapeutic manufacturing, regulatory development and clinical testing.
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Publications
See current publications list at PubMed and Research Gate profile.
Education
The Cardiac Translational Research Laboratory provides research training to undergraduate, graduate and postdoctoral trainees interested in translational cardiovascular science. Trainees participate directly in hypothesis-driven research spanning molecular and cellular biology, human cardiac models, extracellular-vesicle biology, cardiac electrophysiology, preclinical disease models and therapeutic development.
Regular laboratory meetings, research presentations and journal clubs provide opportunities for scientific discussion, critical appraisal, collaborative problem-solving and professional development. Dr. Davis also contributes to undergraduate and graduate teaching in cardiovascular biology and clinical and translational medicine at the University of Ottawa.
Focus
Atrial fibrillation and biological therapeutics
A major translational program in the laboratory is focused on developing new biological therapies for atrial fibrillation. We have pioneered the use of human heart-derived extracellular vesicles as a potential disease-modifying therapy that targets the inflammatory and fibrotic substrate responsible for atrial fibrillation rather than simply suppressing the arrhythmia.
Our research investigates extracellular-vesicle uptake and biodistribution, NLRP3 inflammasome and caspase-1 signalling, atrial inflammation and fibrosis, postoperative atrial fibrillation, and local and systemic approaches to extracellular vesicle delivery. The program spans human cardiac cells and tissues, small- and large-animal models, GMP-compatible manufacturing, preclinical safety and efficacy testing, regulatory development and translation toward first-in-human clinical trials.
Inflammatory heart disease and cardiac sarcoidosis
The laboratory studies how myocardial inflammation produces cardiac injury, fibrosis and arrhythmias. Cardiac sarcoidosis is a major focus of this work. We developed the first acquired experimental model of cardiac sarcoidosis, providing a platform to investigate the mechanisms responsible for myocardial inflammation and fibrosis and to identify biomarkers and potential therapeutic targets.
This program combines mechanistic studies with experimental models and human disease to better understand inflammatory cardiomyopathies and develop more precise approaches to their diagnosis and treatment.
Cardiac aging and repair
A third major research program examines the mechanisms responsible for age-related deterioration of cardiac function and the biological pathways that regulate myocardial repair. This work seeks to identify therapeutic approaches capable of preserving cardiac health with aging and restoring endogenous repair pathways.
Translational approach
The laboratory brings together molecular and cellular biology, cardiac electrophysiology, extracellular-vesicle biology, human cardiac tissue, small- and large-animal disease models and therapeutic development. This integrated approach allows discoveries made at the laboratory bench to be tested in clinically relevant systems and, where warranted, advanced through manufacturing and regulatory development toward clinical trials.
Our goal is not simply to describe cardiovascular disease, but to use mechanistic insight to create and test new treatments for patients.