Phyllis Billia
MD, PhD, FRCPC, University of Toronto
Appointments
- Director of Research, Peter Munk Cardiac Centre
- Medical Director, Mechanical Circulatory Support Program
- Co-director, Peter Munk Cardiovascular Biobank
- Assistant Professor, University of Toronto
At A Glance
- Heart failure is the leading cause of morbidity and mortality in North America and has been identified as the second leading cause of extended hospital stays.
- In the adult, cardiomyocytes are post-mitotic terminally differentiated cells that are unable to proliferate. This renders the heart particularly vulnerable to injury. While cell-based therapies continue to attract considerable interest, they are sufficiently problematic. As such, it is exceedingly important to consider alternative approaches that allow the discovery of novel treatment strategies to effectively maintain tissue homeostasis and restrict cardiomyocyte loss.
- Tumour suppressors and coaxing the heart back into a proliferative state for the regulation of normal tissue homeostasis.
- Our concept of preventing cardiomyocyte loss is through the regulation of the cell cycle, either by altering tumour suppressor genes or providing a permissive environment for proliferation, to allow the heart to undergo repair at the site of injury and maintain tissue homeostasis.
Short Bio
Dr. Billia is a member of the Division of Cardiology at the University Health Network and a Scientist at the Toronto General Research Institute. She completed her medical and research training at the University of Toronto and she is a graduate of the Medical Biophysics PhD program. Recently she completed a post-doctoral fellowship with the world-renowned Dr. Tak W. Mak at the Campbell Family Institute for Cancer Research. She currently is the co-Director of the Peter Munk Cardiovascular Biobank and Medical Director of the Mechanical Circulatory Assist Program. She has embarked on her own research career with funding from the Canadian Institutes of Health Research, focusing on understanding the molecular underpinnings of disease progression in patients with heart failure. In particular, her laboratory is examining how tumor suppressors and regulators of metabolism can coax the terminally differentiated cardiomyocyte back into cell cycle to provide a potential for repair post-injury. She also has an interest in disease modeling in a dish using induced pluripotent stem cell technology.