Co-Mentor: Mark Nash, PhD
Health benefits of exercise are numerous and well established. Beyond counteracting age-related musculoskeletal system wasting, exercise can prevent or mitigate many cardiovascular, metabolic and neurological diseases. While resistance training increases muscle mass and strength, endurance exercise provides long-term benefit to many systems including the cardiovascular system, the immune system, the brain and the adipose tissue.
We are taking an integrative systems biology approach, building comprehensive multi-dimensional molecular maps of exercise response and identifying and validating signaling pathways and molecular mediators of the effect of exercise. In collaboration with our academic partners (Massachusetts General Hospital, USA and The University of Leicester, UK), we have generated large-scale molecular profiles of exercising human subjects and rodent models (Transcriptomics, Somascan proteomics, phospho-proteomics, metabolimic etc...) including careful clinical or pre-clinical assessment (fitness endpoints includes for example: BMI, muscle strength, Vo2max, insulin resistance, etc.). We use a palette of computational biology methods, including causal reasoning, modeling, Grammatical Evolution Neural Networks and knowledge graphs, to integrate these data and derive novel hypotheses testable in the laboratory. Our group works in close collaboration with wet-lab experts, and uses innovative computational approaches to combine and contextualize data from state-of-the-art exercise-relevant systems. We recently discovered and confirmed that in vivo modulation of microglia in the spinal cord is a direct consequence of running and counteracts age-related phenotypes.
GDF11 Increases with Age and Inhibits Skeletal Muscle Regeneration.
Egerman MA, Cadena SM, Gilbert JA, Meyer A, Nelson HN, Swalley SE, Mallozzi C, Jacobi C, Jennings LL, Clay I, Laurent G, Ma S, Brachat S, Lach-Trifilieff E, Shavlakadze T, Trendelenburg AU, Brack AS, Glass DJ.
Cell Metab. 2015 Jul 7;22(1)
Genomic profiling reveals that transient adipogenic activation is a hallmark of mouse models of skeletal muscle regeneration.
Lukjanenko L, Brachat S, Pierrel E, Lach-Trifilieff E, Feige JN.
PLoS One. 2013 Aug 15;8(8)
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