ReviewDisease models & mechanisms2020
Fibrodysplasia ossificans progressiva: current concepts from bench to bedside.
Review in Disease models & mechanisms, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- PJ34 Prevents Trauma-Induced Heterotopic Ossification without Adverse Bone Healing: An in vivo and in vitro Investigation.Drug design, development and therapy · 2026Article
- A Narrative Review of Phase II and III Clinical Trials for the Pharmacological Treatment of Fibrodysplasia Ossificans Progressiva (FOP): Efficacy, Safety, and Challenges in Treatment Strategies.Drug design, development and therapy · 2025Review
- Review
- ACVR mutation [NM_001105.4:c.774G>T (p.Arg258Ser)] in pediatric fibrodysplasia ossificans progressiva complicated by scoliosis: a case report.Frontiers in pediatrics · 2025Article
- Challenges in the diagnosis of fibrodysplasia ossificans progressiva with the ACVR1 mutation (c.774G > C, p.R258S): a case report and review of literature.Orphanet journal of rare diseases · 2024Review
- Immunologic Aspects in Fibrodysplasia Ossificans Progressiva.Biomolecules · 2024Review
- Review
- Momelotinib (JAK1/JAK2/ACVR1 inhibitor): mechanism of action, clinical trial reports, and therapeutic prospects beyond myelofibrosis.Haematologica · 2023Article
- Development of an Animal Model for Traumatic Brain Injury Augmentation of Heterotopic Ossification in Response to Local Injury.Biomedicines · 2023Article
- High Bone Mass Disorders: New Insights From Connecting the Clinic and the Bench.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Review
- The terminal period findings of late-diagnosed fibrodysplasia ossificans progressiva.German medical science : GMS e-journal · 2023Article
- Characterization of Fibrodysplasia Ossificans Progessiva relevant Acvr1/Acvr2 Activin receptors in medaka (Oryzias latipes).PloS one · 2023Article
- Myositis Ossificans with Aneurysmal Bone Cystic Changes at the Thoracic Paraspinal Region: A Case Report.Medicina (Kaunas, Lithuania) · 2022Article
- Heterotopic Ossification: Clinical Features, Basic Researches, and Mechanical Stimulations.Frontiers in cell and developmental biology · 2022Review
- A case of Fibrodysplasia Ossificans Progressiva associated with a novel variant of the ACVR1 gene.Molecular genetics & genomic medicine · 2021Article
- Article
- Heterotopic ossification in mice overexpressing Bmp2 in Tie2+ lineages.Cell death & disease · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heterotopic ossification (HO) is a disorder characterised by the formation of ectopic bone in soft tissue. Acquired HO typically occurs in response to trauma and is relatively common, yet its aetiology remains poorly understood. Genetic forms, by contrast, are very rare, but provide insights into the mechanisms of HO pathobiology. Fibrodysplasia ossificans progressiva (FOP) is the most debilitating form of HO. All patients reported to date carry heterozygous gain-of-function mutations in the gene encoding activin A receptor type I (ACVR1). These mutations cause dysregulated bone morphogenetic protein (BMP) signalling, leading to HO at extraskeletal sites including, but not limited to, muscles, ligaments, tendons and fascia. Ever since the identification of the causative gene, developing a cure for FOP has been a focus of investigation, and studies have decoded the pathophysiology at the molecular and cellular levels, and explored novel management strategies. Based on the established role of BMP signalling throughout HO in FOP, therapeutic modalities that target multiple levels of the signalling cascade have been designed, and some drugs have entered clinical trials, holding out hope of a cure. A potential role of other signalling pathways that could influence the dysregulated BMP signalling and present alternative therapeutic targets remains a matter of debate. Here, we review the recent FOP literature, including pathophysiology, clinical aspects, animal models and current management strategies. We also consider how this research can inform our understanding of other types of HO and highlight some of the remaining knowledge gaps.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.