Our laboratory investigates how metabolic, epigenetic, and stem cell programs coordinate tissue development, regeneration, and homeostasis in health and disease. We are particularly interested in mitochondria and lipid droplets, and in how their signaling and metabolite outputs communicate with the nucleus to regulate gene expression and cell fate. Using skeletal muscle and adipose tissue as model systems, we study how metabolic and epigenetic remodeling influences stem and progenitor cell function, tissue regeneration, and organ physiology, and how its dysregulation contributes to aging, muscle degeneration, obesity and diabetes. Our work integrates transgenic and preclinical mouse models, primary human cells, single-cell multiomics, high-resolution imaging, and biochemical and bioenergetic analyses to define how mitochondrial remodeling, lipid metabolism, and chromatin regulation control stem cell activity and tissue homeostasis. Ultimately, these studies aim to advance therapeutic strategies for metabolic disease, regenerative medicine, and healthy aging.
Molecular control of muscle stem cell fate and function
Muscle stem cell, also called satellite cell, is responsible for skeletal muscle growth, maintenance and repair. Satellite cell undergoes fate transitions between quiescence, activation, self-renewal and differentiation during maintenance and regeneration. Disruptions of this homeostasis compromise stem cell function and cause muscle wasting or regenerative failure. The main research interest of the lab is the mechanisms underlying the sophisticated fate decision-making processes. A major focus of our ongoing studies is to understand how cellular metabolism coordinates with epigenetic landscape and stem cell niche to regulate their behavior. We are also exploring novel signaling molecules that regulate the maintenance and function of muscle stem cell.
Nutritional/metabolic regulation of muscle development and growth
Skeletal muscle, which accounts for 40 percent of our body mass, is a highly heterogeneous tissue playing critical roles in maintaining body motility and systemic energy homeostasis. We are interested in the molecular and cellular basis that determines muscle formation and maturation, in particular the regulation of nutritional signaling and metabolic pathways on muscle growth. Current studies focus on understanding how nutrient and exercise remodel mitochondrial integrity and function to affect muscle growth and function in physiological and pathological conditions.
Molecular and cellular mechanisms underlying adipogenesis
Adipose tissue is a central metabolic organ in regulating whole-body energy homeostasis. White adipose tissue functions as a major energy reservoir and brown adipose tissue stores lipids for adaptive thermogenesis. Adipocytes resided in different anatomical adipose depots execute divergent origins and physiological functions throughout animal’s lifespan. In response to changes of nutritional conditions or cold exposure, adipose tissue undergoes dynamic remodeling for metabolic requirement which governed by complicated molecular and cellular regulatory signaling. One of our research interests is the molecular and cellular mechanisms underlying adipogenesis, particularly the formation of intramuscular adipocyte.
Pathogenesis and therapy of neuromuscular diseases
Muscular dystrophy is a group of genetic diseases that cause progressive muscle degeneration and weakness and loss of muscle mass with or without the damage of nerve tissue. Duchenne muscular dystrophy (DMD) is the most common type, caused by inherited mutations in the X-linked dystrophin gene. We are studying the primary pathogenesis of DMD with a preclinical mdx mouse model that recapitulates human pathophysiology. We focus on developing new strategies to boost the regrowth of damaged muscle and increase muscle strength in DMD, with the ultimate goal to improve the life quality and survival of patient.
YUE LABORATORY 