Skeletal muscles account for a significant proportion of total body mass and are essential for locomotion, posture, breathing, thermogenesis, and whole-body metabolism. Given its abundance and the diverse range of critical functions it performs, it is not surprising that muscle mass and function are closely linked to overall health. Muscle tissue is composed of metabolically diverse types of muscle fibers that respond differently to exercise, aging, and disease. The loss of skeletal muscle mass (atrophy) is a common consequence of numerous clinical conditions, including cancer, muscular dystrophy, sepsis, multiple sclerosis, and aging. Despite its significant clinical impact, the underlying molecular mechanisms regulating skeletal muscle mass remain incompletely understood.
The goal of JPLG Muscle Physiology Lab is to dedicated to the study and improvement of skeletal muscle health. Our current research focuses on understanding cellular and molecular processes that regulated skeletal muscle integrity, identifying therapeutic targets, and developing strategies to improve muscle health across a range of conditions.
Overview of current research projects
Investigating the role of Autophagy and Mitophagy in skeletal muscle healh.
Our lab is focused on unraveling the molecular mechanisms underpinning the complex relationship between inflammation and autophagy signaling in aging, metabolic disorders, and in neuromuscular diseases.
Our research lab interests also include characterizing novel genes involved in autophagy signaling with the goal of advancing fundamental knowledge and improving overall health.
Investigating new mechanisms of action of exercise-induced skeletal muscle adaptation.
Investigating the role of peroxisomes in regulating skeletal muscle mass and function in response to atrophic stimuli.
The JPLG lab also study the role of mitochondrial dysfunction, a common underlying feature of many muscle-wasting conditions, including disuse-induced atrophy, sarcopenia, and neuromuscular diseases. The lab focuses on examining how mitochondrial bioenergetic defects and mitophagy impairments contribute to the progression of muscle-wasting diseases.
Figure Reference: Made by JP Leduc-Gaudet with Biorender