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Journal of Zhejiang University SCIENCE B 1998 Vol.-1 No.-1 P.

http://doi.org/10.1631/jzus.B2300779


Advancements in mechanisms and drug treatments for fibrodysplasia ossificans progressiva


Author(s):  Yijun ZHOU, Ce SHI, Hongchen SUN

Affiliation(s):  Department of Endodontics, Hospital of Stomatology, Jilin University, Changchun, 130021, China; more

Corresponding email(s):   hcsun@jlu.edu.cn, ceshi@jlu.edu.cn

Key Words:  Fibrodysplasia ossificans progressive (FOP), Heterotopic ossification (HO), Mechanism, Drug treatment, Activin A receptor type 1 (ACVR1)


Yijun ZHOU, Ce SHI, Hongchen SUN. Advancements in mechanisms and drug treatments for fibrodysplasia ossificans progressiva[J]. Journal of Zhejiang University Science B, 1998, -1(-1): .

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Abstract: 
Fibrodysplasia ossificans progressiva (FOP) is a rare genetic disorder characterized by congenital bilateral malformation of the large toe and progressive, extensive, and irreversible heterotopic ossification (HO) of soft tissues throughout the body, leading to severe disabilities. FOP is caused primarily by mutations in activin A receptor type I (ACVR1), also known as activin-like kinase 2 (ALK2), a receptor belonging to the bone morphogenetic protein (BMP) type I family. However, the continuous and complex process of HO in FOP is not yet fully understood, which has impeded the development of therapeutic drugs. Despite surgical removal of HO, which often results in recurrence and expansion of ossification, there is currently no definitive drug treatment available to completely prevent, halt, or reverse the progression of HO in FOP. Currently, researchers are intensively studying the pathogenesis of FOP at various stages and developing promising drug candidates, including Saracatinib, Palovarotene, and Rapamycin. This review provides an overview of progress in understanding the mechanism of FOP and the development of therapeutic drugs, with the goal of providing insights for further research and the development of new treatment methods.

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