My overarching research goals are to better understand the cellular and molecular mediators of fracture healing and bone adaptation, with a special interest on crosstalk mechanisms from neighboring skeletal muscle and immune cells. My primary research interest arises from the large body of clinical and preclinical evidence that impaired fracture healing occurs in conditions of altered mechanosensation such as disuse, aging or fixation failure and excess pathological inflammation (osteoporosis, diabetes) or muscle injury (polytrauma). To better understand the mechanisms regulating fracture healing during these disease states, my lab utilizes cutting-edge in vivo and in vitro loading models (axial compression, substrate stretch/shear by fluid flow, hindlimb unloading), muscle loading (optogenetics; electrical stimulation), molecular endpoints (histology, RNAseq) and computational modeling (finite element virtual mechanical testing) in genetically altered animals and immortalized cell lines from skeletal muscle, bone and immune cells. We foster to create an inclusive and nurturing lab environment where people feel seen and valued and can grow throughout their research and professional training via personalized training plans.

Accepting students per funding availability; please inquire directly if interested.

Joining UC Davis July 2025