Grant: Doctoral Research Award: Canada Graduate Scholarships

Duchenne muscular dystrophy (DMD) is a genetic disorder that causes muscles to weaken and waste away over time, leading to challenges in moving, breathing, and performing daily activities. DMD is caused by mutations in a gene called dystrophin, which plays crucial structural and functional roles in muscle. Without it, muscle repair becomes inefficient, especially as cells responsible for muscle regeneration, called muscle stem cells, lose their ability to function properly. Currently, there is no cure for DMD and treatments aim only to slow down muscle deterioration. Recent discoveries in genetics have identified molecules called non-coding RNAs (ncRNAs) which are powerful regulators of gene activity and cell behavior. Unlike messenger RNAs, ncRNAs do not produce proteins. Instead, they act as "switches" to control other genes, including those involved in muscle repair. These ncRNAs could provide new therapeutic pathways for DMD. This project will explore the role of specific ncRNAs in muscle stem cell function and examine whether they can be manipulated to restore a healthier balance of muscle repair in DMD. By studying the differences in ncRNA profiles between healthy vs. DMD-derived muscle stem cells, we aim to identify ncRNAs that promote muscle repair and improve muscle strength in a DMD mouse model. This research could lead to new DMD treatments that target ncRNAs for improved muscle repair. Such treatments could ultimately help individuals with DMD experience greater muscle function, strength, and quality of life. The results could also expand therapeutic strategies for other muscle-wasting diseases, enhancing personal and population health outcomes for those affected.