ReviewCells2020
The Survey of Cells Responsible for Heterotopic Ossification Development in Skeletal Muscles-Human and Mouse Models.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Periprosthetic joint infection and heterotopic ossification after total hip arthroplasty: systematic review and meta-analysis.BMC musculoskeletal disorders · 2025Pooled it
- Heterotopic Ossification: Molecular Drivers, Subtype-Specific Mechanisms, and Translational Therapeutic Advances.Biomolecules · 2026Review
- Carnosic acid serves as a dual Nrf2 activator and PTEN/AKT suppressor to inhibit traumatic heterotopic ossification.Stem cell research & therapy · 2025Article
- CBD-conjugated BMP-inhibiting exosomes on collagen scaffold dual-target Achilles tendon repair: Synergistic regeneration and heterotopic ossification prevention.Materials today. Bio · 2025Article
- Genetic regulation of injury-induced heterotopic ossification in adult zebrafish.Disease models & mechanisms · 2024Article
- KLF2/PPARγ axis contributes to trauma-induced heterotopic ossification by regulating mitochondrial dysfunction.Cell proliferation · 2024Article
- BMP-2 promotes fracture healing by facilitating osteoblast differentiation and bone defect osteogenesis.American journal of translational research · 2023Article
- The role of miRNA and lncRNA in heterotopic ossification pathogenesis.Stem cell research & therapy · 2022Review
- Are there really specific risk factors for heterotopic ossifications? A case report of 'non-risk factor' after total hip replacement.The Journal of international medical research · 2022Article
- BMP signaling and skeletal development in fibrodysplasia ossificans progressiva (FOP).Developmental dynamics : an official publication of the American Association of Anatomists · 2022Review
- Heterotopic ossification in mice overexpressing Bmp2 in Tie2+ lineages.Cell death & disease · 2021Article
- MyD88 Is Not Required for Muscle Injury-Induced Endochondral Heterotopic Ossification in a Mouse Model of Fibrodysplasia Ossificans Progressiva.Biomedicines · 2021Article
- Heterotopic ossification in a patient with diffuse idiopathic skeletal hyperostosis: Input from histological findings.European journal of histochemistry : EJH · 2020Article
- When the Nervous System Turns Skeletal Muscles into Bones: How to Solve the Conundrum of Neurogenic Heterotopic Ossification.Current osteoporosis reports · 2020Review
- Fibrodysplasia ossificans progressiva: current concepts from bench to bedside.Disease models & mechanisms · 2020Review
- Muscle Homeostasis and Regeneration: From Molecular Mechanisms to Therapeutic Opportunities.Cells · 2020Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heterotopic ossification (HO) manifests as bone development in the skeletal muscles and surrounding soft tissues. It can be caused by injury, surgery, or may have a genetic background. In each case, its development might differ, and depending on the age, sex, and patient's conditions, it could lead to a more or a less severe outcome. In the case of the injury or surgery provoked ossification development, it could be, to some extent, prevented by treatments. As far as genetic disorders are concerned, such prevention approaches are highly limited. Many lines of evidence point to the inflammatory process and abnormalities in the bone morphogenetic factor signaling pathway as the molecular and cellular backgrounds for HO development. However, the clear targets allowing the design of treatments preventing or lowering HO have not been identified yet. In this review, we summarize current knowledge on HO types, its symptoms, and possible ways of prevention and treatment. We also describe the molecules and cells in which abnormal function could lead to HO development. We emphasize the studies involving animal models of HO as being of great importance for understanding and future designing of the tools to counteract this pathology.
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.