LAUSR

only three anabolic drugs that induce bone formation are currently approved for the treatment of osteoporosis. Furthermore, existing agents cannot be used for long treatment periods and are associa­ ted with severe adverse effects. A new study in Cell Reports now identifies fibroblast activation protein (FAP) as a suppressor of osteogenesis and potential anti­osteoporosis drug target. “I previously discovered a novel osteogenic growth factor called osteolectin and wanted to dissect the mechanisms underlying its osteogenic activity, which led to the identification of FAP as its interacting partner and the current paper,” explains corresponding author Rui Yue. First, in vitro assays were carried out to identify proteins that co-precipitated with osteolec­ tin, leading to the discovery of the glycoprotein FAP as an interactor. Further in vitro overexpression studies demonstrated that osteolectin notably inhibits the protease activity of FAP. In addition, experiments carried out in zebrafish showed that osteolectin induces bone mineralization by inhibiting FAP. In vivo studies in Fap­deficient mice showed ameliorated loss of trabecular bone in the limbs during ageing com­ pared with littermate control mice. B O n E