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• W3045572912 endingPage "115539" @default.
• W3045572912 startingPage "115539" @default.
• W3045572912 abstract "Fibrodysplasia ossificans progressiva (FOP) is an ultra-rare genetic disorder of extraskeletal bone formation, but could appropriately be viewed as a seminal disorder of osteochondrogenesis. Many, if not most, of the musculoskeletal features of FOP are related to dysregulated chondrogenesis including abnormal articular cartilage formation, abnormal diarthrodial joint specification, growth plate dysplasia, osteochondroma formation, heterotopic endochondral ossification (HEO), and precocious arthropathy. In FOP, causative activating mutations of Activin receptor A type I (ACVR1), a bone morphogenetic protein (BMP) type I receptor, are responsible for the osteochondrodysplasia that impacts developmental phenotypes as well as postnatal features of this illustrative disorder. Here, we highlight the myriad developmental and postnatal effects on osteochondrogenesis that emanate directly from mutant ACVR1 and dysregulated bone morphogenetic protein (BMP) signaling in FOP." @default.
• W3045572912 created "2020-08-03" @default.
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• W3045572912 date "2020-11-01" @default.
• W3045572912 modified "2023-09-25" @default.
• W3045572912 title "Fibrodysplasia ossificans progressiva (FOP): A disorder of osteochondrogenesis" @default.
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• W3045572912 doi "https://doi.org/10.1016/j.bone.2020.115539" @default.
• W3045572912 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7502483" @default.
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