A molecule secreted from young, but not old, blood cells can speed up fracture healing in elderly mice, reports a paper published in Nature Communications this week. Although the exact chemical nature of the molecule remains to be identified, the study could help to explain why fractures take longer to heal in old individuals and points out a potential path for the development of drugs that promote fracture healing.
The reparative capacity of tissues declines with age and this is reflected in the increased time it takes for fractures to heal in the elderly, but the molecular mechanisms responsible for this age-dependent decline are incompletely understood.
Benjamin Alman and colleagues now show that blood cells circulating in young mice secrete a molecule that increases the regenerative capacity of bone cells. They determined this by connecting the circulation of young and old animals and conducting bone-marrow transplants, which allowed them to demonstrate that a specific molecule, which may be either a chemical or a small protein, is only secreted from young blood cells. This molecule works by reducing levels of the signalling molecule beta-catenin in bone cells called osteoblasts and the authors discovered that this was associated with the formation of new bone of higher density.