Abstract
Fibrodysplasia ossificans progressiva (FOP) is a rare and illustrative genetic disorder in which bone forms episodically in soft connective tissues during childhood and throughout adult life, often in response to injury. The extraskeletal bone in FOP develops through endochondral ossification and is caused by activating mutations in ACVR1, the gene encoding the ALK2 BMP type I receptor, that enhance activation of the bone morphogenetic protein (BMP) signaling pathway. The identification of the causative gene in FOP, together with the development of animal models for heterotopic ossification and FOP, have stimulated rapid advances in understanding the cellular and molecular mechanisms of bone formation and the pathological induction of heterotopic ossification. This knowledge leads to the development of novel therapeutic approaches to inhibit BMP signaling and heterotopic ossification.
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