Project 458860
Large-scale study of patient-specific phenotypical, functional and proteomic differences in induced pluripotent stem cell-derived cardiomyocytes after hypoxic injury
Large-scale study of patient-specific phenotypical, functional and proteomic differences in induced pluripotent stem cell-derived cardiomyocytes after hypoxic injury
Project Information
| Study Type: | Unclear |
| Research Theme: | Biomedical |
Institution & Funding
| Principal Investigator(s): | Derish, Ida |
| Supervisor(s): | Cecere, Renzo |
| Institution: | Research Institute of the McGill University Health Centre |
| CIHR Institute: | Circulatory and Respiratory Health |
| Program: | |
| Peer Review Committee: | Doctoral Research Awards - A |
| Competition Year: | 2021 |
| Term: | 3 yrs 0 mth |
Abstract Summary
Heart attacks remain a leading cause of death worldwide and a major burden on the healthcare system, despite recent advances in medicine. During a heart attack, damage to heart cells can occur from a stop of blood flow and a subsequent oxygen restriction, often causing irreparable harm or cell death. Unfortunately, muscle cells of the heart cannot regenerate on their own once they have been damaged, leaving patients with a chronic disease called heart failure and a limited number of treatment options. Moreover, pharmacological developments in the field of heart repair yield high rates of unforeseen side effects and great variability between patient treatment outcomes. This is due to a lack of a representative heart model to reliably account for the drug response diversity in a population. Furthermore, drugs that treat cardiovascular diseases are not patient-specific, highlighting the field's limited progress towards personalized medicine. While the use of stem cell-derived heart cells has gained traction as a superior and easily replenishable cell source, patient-specific differences remain poorly understood and understudied. Our project explores the usage of stem cell-derived heart cells as a model to monitor patient differences in response to cellular injury. Since the cells all contain the patient's genetic code, these cells can then be tested upon and will reflect their donor's distinct outcomes - including their responses to injury and experimental heart repair drugs - outside of the patient's body. Specifically, our study involves generating heart cells from the blood of healthy donors and diseased patients, subjecting them to oxygen deprivation and mimicking a heart attack injury. This study provides the groundwork to understanding patient-specific differences via this cellular practical tool, paving way to the screening for safe and effective therapies and thus upholding a higher standard of care for heart failure patients.
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