Restoring muscle regeneration in disease and aging
Our goal is to understand why muscle sometimes fails to regenerate in disease, and how to restore the repair mechanism when it does break down. We study muscle stem cells and the environments they live in, focusing on how inflammatory signals and epigenetic mechanisms determine whether regeneration succeeds or fails.
Research Focus
Overview
Skeletal muscle has a remarkable capacity to regenerate, driven by a population of resident stem cells known as satellite cells. This regenerative capacity is essential for growth, repair after injury, and the maintenance of muscle mass throughout life. In many diseases, including muscular dystrophies, and during aging, this process breaks down. Muscle stem cells fail to properly activate, expand, or differentiate, leading to progressive loss of muscle function. Our work aims to understand why this failure occurs. We focus on how the local environment—particularly inflammatory signals—interacts with epigenetic mechanisms to control gene expression programs in muscle stem cells. By identifying how these programs become disrupted, we seek to develop strategies to reprogram stem cells and restore effective regeneration.
Current Questions
Why does regeneration fail?
What changes in muscle stem cells and their environment cause repair to break down in disease and aging?
Can we reset dysfunctional stem cells?
Are the defects in muscle stem cells permanent, or can we reprogram their epigenetics to restore regenerative function?
How does inflammation shape regeneration?
How much inflammation is needed to support repair, and at what point does it push stem cells toward failure?
How is gene expression rewritten during regeneration?
How do stem cells transition between states and establish new gene expression programs required to form functional muscle fibers?
Do cells “remember” injury?
Do stem cells retain epigenetic memory of past inflammation or damage, and how does that affect future regeneration?
Can we target epigenetics therapeutically to improve regeneration?
Can we manipulate chromatin regulators to improve regeneration in muscular dystrophy and age-related muscle loss?
