ReviewAnnals of the New York Academy of Sciences2011
Fibrodysplasia ossificans progressiva: a blueprint for metamorphosis.
Review in Annals of the New York Academy of Sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 38 citations in OpenAlex.
- Genetic regulation of injury-induced heterotopic ossification in adult zebrafish.Disease models & mechanisms · 2024Article
- Study methodology and insights from the palovarotene clinical development program in fibrodysplasia ossificans progressiva.BMC medical research methodology · 2023Article
- Living with Fibrodysplasia Ossificans Progressiva: Radiological Images of a Patient with Extensive Heterotopic Ossification.Diagnostics (Basel, Switzerland) · 2023Article
- Heterotopic ossification vs. fracture healing: Extracellular vesicle cargo proteins shed new light on bone formation.Bone reports · 2022Article
- Challenges and Opportunities for Drug Repositioning in Fibrodysplasia Ossificans Progressiva.Biomedicines · 2021Review
- Fibrodysplasia Ossificans Progressiva: What Have We Achieved and Where Are We Now? Follow-up to the 2015 Lorentz Workshop.Frontiers in endocrinology · 2021Review
- Fibrodysplasia ossificans progressiva: current concepts from bench to bedside.Disease models & mechanisms · 2020Review
- Application of human induced pluripotent stem cells to model fibrodysplasia ossificans progressiva.Bone · 2018Review
- Novel Model of Tendon Regeneration Reveals Distinct Cell Mechanisms Underlying Regenerative and Fibrotic Tendon Healing.Scientific reports · 2017Article
- The protein kinase LKB1 negatively regulates bone morphogenetic protein receptor signaling.Oncotarget · 2016Article
- Muscle-bone interactions during fracture healing.Journal of musculoskeletal & neuronal interactions · 2015Review
- Unique genetic and epigenetic mechanisms driving paediatric diffuse high-grade glioma.Nature reviews. Cancer · 2014Review
- The phenotype and genotype of fibrodysplasia ossificans progressiva in China: a report of 72 cases.Bone · 2013Article
- The skeleton in the closet.Gene · 2013Article
- From mysteries to medicines: drug development for fibrodysplasia ossificans progressive.Expert opinion on orphan drugs · 2013Article
- The role of muscle in bone repair: the cells, signals, and tissue responses to injury.Current osteoporosis reports · 2013Review
- Overactive bone morphogenetic protein signaling in heterotopic ossification and Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2013Review
- Fibrodysplasia ossificans progressiva: mechanisms and models of skeletal metamorphosis.Disease models & mechanisms · 2012Review
- [Is there a place in primary care for rare diseases? The case of fibrodysplasia ossificans progressiva].Atencion primariaArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The most important milestone in understanding a genetic disease is the identification of the causative mutation. However, such knowledge is often insufficient to decipher the pathophysiology of the disorder or to effectively treat those affected. Fibrodysplasia ossificans progressiva (FOP) is a rare, disabling, genetic disease of progressive heterotopic endochondral ossification (HEO) enabled by missense mutations that promiscuously and provisionally activate ACVR1/ALK2, a bone morphogenetic protein (BMP) type I receptor, in all affected individuals. While activating mutations of the ACVR1/ALK2 receptor are necessary, disease activity and progression also depend on altered cell and tissue physiology. Recent findings identify inflammatory and immunological factors, vascular-derived mesenchymal stem cells, and a hypoxic lesional microenvironment that trigger, promote, and enable episodic progression of FOP in the setting of the genetic mutation. Effective therapies for FOP will need to consider these seminal pathophysiologic interactions.
Indexed as
Identifiers
What OpenQuestion holds
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.