Fibrodysplasia ossificans progressiva (FOP), characterized by extra bone formation in soft tissues, is caused by a gain-of-function mutation in ACVR1, a transmembrane receptor. Recently, a potential treatment was developed by identifying a novel molecular mechanism underlying bone formation in FOP. These findings have opened the door to beating FOP.
Keywords: activin; bone morphogenetic protein (BMP); heterotopic ossification; intracellular signaling; ligand; receptor.
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