Our Research
Our laboratory studies the biological mechanisms that create arrhythmogenic cardiac disease and uses those insights to develop new therapeutic approaches.
We are developing heart-derived extracellular vesicles as a disease-modifying biological therapy for atrial fibrillation, with a particular focus on inflammation, fibrosis and the atrial substrate that permits AF to occur.
Learn about the AF program →Our work connects mechanistic discovery with human cells, preclinical disease models, large-animal studies and GMP-compatible manufacturing approaches designed to move biological therapies toward clinical testing.
See our translational research →We investigate inflammatory mechanisms responsible for myocardial injury and arrhythmias in cardiac sarcoidosis, with the goal of identifying new disease mechanisms and therapeutic targets.
Explore cardiac sarcoidosis →A Different Approach to Atrial Fibrillation
Contemporary AF therapies primarily target the electrical manifestation of the disease. Our laboratory is exploring a different possibility: whether biological therapy can alter the inflammatory and fibrotic atrial substrate that allows atrial fibrillation to develop and persist.
Heart-derived extracellular vesicles carry bioactive signals capable of modifying inflammatory and profibrotic pathways. We are defining how these vesicles interact with the diseased atrium and how that biology can be translated into a practical therapeutic strategy.
Read the science behind the approach →
Featured Research
Our recent work demonstrates the potential of targeted, clinical-grade extracellular vesicle therapy to prevent inflammation-driven postoperative atrial fibrillation.
Targeted delivery of human cardiac extracellular vesicles prevented spontaneous postoperative atrial fibrillation in treated animals and attenuated atrial inflammatory and fibrotic remodeling in a clinically relevant porcine model.
Read the paper →