ReviewBritish journal of clinical pharmacology2019
Therapeutic advances for blocking heterotopic ossification in fibrodysplasia ossificans progressiva.
Review in British journal of clinical pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
36 citing papers in PubMed, 68 citations in OpenAlex.
- Single-base 2'OMe-modified LNA and MOE gapmers selectively silenceMolecular therapy. Nucleic acids · 2026Article
- Precision RNAi for Fibrodysplasia Ossificans Progressiva: a combinatorial, unimolecular, allele selective approach.Research square · 2026Article
- USP24-dependent STAT2 stabilization mediates physiologic and pathologic bone formation.Cell death & disease · 2026Article
- Advancements in mechanisms and drug treatments for fibrodysplasia ossificans progressiva.Journal of Zhejiang University. Science. B · 2025Review
- Fibroblasts in heterotopic ossification: mechanisms and therapeutic targets.International journal of biological sciences · 2025Review
- Role of the NF-kB signalling pathway in heterotopic ossification: biological and therapeutic significance.Cell communication and signaling : CCS · 2024Review
- Pay Attention to the Osteochondromas in Fibrodysplasia Ossificans Progressiva.Orthopaedic surgery · 2024Article
- How Activin A Became a Therapeutic Target in Fibrodysplasia Ossificans Progressiva.Biomolecules · 2024Review
- Review
- Fibrodysplasia ossificans progressiva.Clinical case reports · 2023Article
- AAV-Mediated Targeting of the Activin A-ACVR1Biomolecules · 2023Article
- Novel Therapeutic Targets for Fibrodysplasia Ossificans Progressiva: Emerging Strategies and Future Directions.Cureus · 2023Review
- Suppression of heterotopic ossification in fibrodysplasia ossificans progressiva using AAV gene delivery.Nature communications · 2022Article
- Contemporary perspectives on heterotopic ossification.JCI insight · 2022Review
- Palovarotene: First Approval.Drugs · 2022Review
- Fibrodysplasia ossificans progressiva: A rare disease with spinal deformity and severe hip dysfunction.Frontiers in pediatrics · 2022Article
- BMP signaling and skeletal development in fibrodysplasia ossificans progressiva (FOP).Developmental dynamics : an official publication of the American Association of Anatomists · 2022Review
- Targeted therapy for pediatric diffuse intrinsic pontine glioma: a single-center experience.Therapeutic advances in medical oncology · 2022Article
- Rare and intractable fibrodysplasia ossificans progressiva shows different PBMC phenotype possibly modulated by ascorbic acid and propranolol treatment.Intractable & rare diseases research · 2021Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Fibrodysplasia ossificans progressiva (FOP) is a rare genetic disease in which heterotopic bone forms in muscle and soft tissue, leading to joint dysfunction and significant disability. FOP is progressive and many patients are wheelchair-bound by the 3rd decade of life. FOP is caused by an activating mutation in the ACVR1 gene, which encodes the activin A Type 1 receptor. Aberrant signalling through this receptor leads to abnormal activation of the pSMAD 1/5/8 pathway and triggers the formation of bone outside of the skeleton. There is no curative therapy for FOP; however, exciting advances in novel therapies have developed recently. Here, we review the clinical and translational pharmacology of three drugs that are currently in clinical trials (palovarotene, REGN 2477 and rapamycin) as well as other emerging treatment strategies for FOP.
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Registered trials
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.