Major research areas:

We previously demonstrated that appropriate regulation of physiological inflammation by regulatory T cells (Tregs) is required for the muscle-specific and organism-level metabolic adaptations and improved performance typical of exercise training. In muscles of Treg-deficient mice, interferon gamma production by other lymphocyte populations is unleashed and drives mitochondrial dysfunction to the detriment of endurance-exercise performance. The Langston Lab aims to build on this foundational work by systematically mapping the multi-cellular responses to exercise in skeletal muscle to identify additional drivers and resistors of adaptation in youth and during aging.

We discovered that mechanical stress ignites muscle inflammation after exercise and injury via stimulation of the mechanosensitive cation channel Piezo1 on mesenchymal stromal cells. We are exploring the immunomodulatory potential of other signals produced after exercise and injury in young and aged muscles.

We have several projects focused on elucidating how exercise protects against and reverses age-related changes in muscle properties (e.g., mass and stiffness) and function.