Premature aging and residual senescence after injury resolution
Bone fractures are one of the most catastrophic events to happen to an older individual. Interestingly, one of the biggest predictors of fracture risk in old age is history of a previous fracture, even as far back as your 20's. During fracture healing in young mice, certain cells within the bone tissue undergo cellular senescence – a process typically specific to old age – and persist beyond the resolution of wound healing. This suggests that previously fractured bones may contain higher levels of senescent cells, thus creating a more “aged” bone that results in faster rates of skeletal aging and higher levels of fracture risk. Dr. Doolittle’s laboratory will test this hypothesis by deeply phenotyping this unique form of senescence and its functional effects on skeletal and organismal aging. Success of this project will implicate skeletal injury as a driver of accelerated aging through a senescence-mediated mechanism.
