Overview
Bursac's research interests include: Stem cell, tissue engineering, and gene based therapies for heart and muscle regeneration; Cardiac electrophysiology and arrhythmias; Organ-on-chip and tissue engineering technologies for disease modeling and therapeutic screening; Small and large animal models of heart and muscle injury, disease, and regeneration.
The focus of my research is on application of pluripotent stem cells, tissue engineering, and gene therapy technologies for: 1) basic studies of striated muscle biology and disease in vitro and 2) regenerative therapies in small and large animal models in vivo. For in vitro studies, micropatterning of extracellular matrix proteins or protein hydrogels and 3D cell culture are used to engineer rodent and human striated muscle tissues that replicate the structure-function relationships present in healthy and diseased muscles. We use these models to separate and systematically study the roles of structural and genetic factors that contribute cardiac and skeletal muscle function and disease at multiple organizational levels, from single cells to tissues. Combining cardiac and skeletal muscle cells with primary or iPSC-derived non-muscle cells (endothelial cells, smooth muscle cells, immune system cells, neurons) allows us to generate more realistic models of healthy and diseased human tissues and utilize them to mechanistically study molecular and cellular processes of tissue injury, vascularization, innervation, electromechanical integration, fibrosis, and functional repair. Currently, in vitro models of Duchenne Muscular Dystrophy, Pompe disease, dyspherlinopathies, and various cardiomyopathies are studied in the lab. For in vivo studies, we employ rodent models of volumetric skeletal muscle loss, cardiotoxin and BaCl2 injury as well as myocardial infarction and transverse aortic constriction to study how cell, tissue engineering, and gene (viral) therapies can lead to safe and efficient tissue repair and regeneration. In large animal (porcine) models of myocardial injury and arrhythmias, we are exploring how human iPSC derived heart tissue patches and application of engineered ion channels can improve cardiac function and prevent heart failure or sudden cardiac death.
Current Appointments & Affiliations
Recent Publications
D801N in ATP1A3-encoded Na/K-ATPase alpha 3 causes cardiac arrhythmogenesis through sodium-calcium exchanger-mediated calcium overload.
Journal Article JCI Insight · April 8, 2026 Short QT syndrome is a heritable arrhythmia disorder linked to sudden cardiac death. We recently identified that individuals with alternating hemiplegia of childhood (AHC), a rare neurodevelopmental disorder, can exhibit shortened corrected QT intervals an ... Full text Link to item CiteExperimental Platform for Screening and Validation of BacNa<sub>v</sub> Gene Therapy Candidates.
Journal Article Circulation. Arrhythmia and electrophysiology · April 2026 Full text CiteRegulation of sodium/calcium homeostasis by BacNa<sub>v</sub> gene therapy rescues cardiac dysfunction in chronic heart failure.
Journal Article Science advances · March 2026 Despite continued progress, therapies to augment contractile function and prevent arrhythmias in patients with heart failure remain limited. Here, we present a two-pronged gene therapy approach that simultaneously augments peak Na+ current and C ... Full text CiteRecent Grants
iPediHeart: Interdisciplinary Research Training Program for Pediatric Heart Disease
Inst. Training Prgm or CMEMentor · Awarded by National Institutes of Health · 2025 - 2030Engineering Heterocellular Human Skeletal Muscle Tissues to Recreate and Study Native Stem Cell Niche Function
ResearchPrincipal Investigator · Awarded by National Institute of Arthritis and Musculoskeletal and Skin Diseases · 2024 - 2029Engineering a Human Skeletal Muscle Tissue Model of LGMD2B
ResearchPrincipal Investigator · Awarded by National Institute of Arthritis and Musculoskeletal and Skin Diseases · 2023 - 2028View All Grants