Associate Professor, Department of Medicine
We study heart disease at varying levels of biological complexity including patients, animal models and individual heart cells to obtain insights into disease mechanisms. We are currently investigating the cellular and molecular mechanisms that cause cardiomyopathy in patients with muscular dystrophy.
Melanie Gartz, MS, MHS
Research Technologist II
Our laboratory is interested in understanding the mechanisms underlying cardiomyopathy, a leading cause of death in patients with Duchenne and Becker muscular dystrophy. Our model system to investigate this phenomenon uses iPS cells differentiated into cardiomyocytes that contain patient specific dystrophin mutations. My role in the laboratory is to maintain our iPS lines and differentiate them into cardiomyocytes for experimentation. Furthermore, I have been investigating the factors contributing to oxidative stress in dystrophic iPS derived cardiomyocytes in order to lead to greater understanding of this unique cardiomyopathy.
Research Technologist I
My primary role within the lab is to provide support for various projects throughout the lab. Currently, my focus is developing in vitro model systems to investigate dystrophic cardiomyopathy and cellular senescence. Techniques I use to support the model systems are maintenance of iPSCs and differentiating them into cardiac and endothelial cells, CRISPR Cas-9 gene editing, and animal behavior studies.
Muhammad Zeeshan Afzal, BPharm, PhD
Dystrophic cardiomyopathy manifested in muscular dystrophy patients is due to mutations of the dystrophin gene, resulting in defective cytoskeletal protein involved in regulation of stretch associated cellular support. My research involves establishing bio-bank of dystrophic patient samples; reprograming of dystrophic patient derived somatic cells into induced pluripotent stem (iPS) cells; and their differentiation into cardiomyocytes. My further investigations focus undertaking fundamental assays to elucidate molecular mechanisms regulating oxidative stress in dystrophic cardiomyocytes and to study their cellular bioenergetics. Our efforts would help establishing basis to understand the oxidative mechanisms contributing towards dystrophic cardiomyopathy.