ArticleJournal of advanced research2026
The IL-1β/NETs/AIM2 axis participates in the formation of trauma-induced heterotopic ossification by orchestrating crosstalk between neutrophils and macrophages.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Tendon stem/progenitor cells in heterotopic ossification: functional regulation, molecular mechanisms and targeted therapeutic strategies.Journal of orthopaedic translation · 2026Review
- The IL-33/ST2 Axis Promotes Traumatic Heterotopic Ossification by Driving Macrophage and Mast Cell-Mediated Inflammation via Autophagy Defects.International journal of biological sciences · 2026Article
- Case Report: Intracranial epidermoid cyst accompanied by bone hyperplasia forming a bone encapsulation.Frontiers in oncology · 2026Article
- Advanced bioactive materials and strategies for tendon repair and function restoration.Journal of orthopaedic translation · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe limitations of clinical treatment for trauma-induced heterotopic ossification (tHO) make it of great significance to fully study its pathogenesis for the treatment of this disease. The infiltration of inflammatory cells, as an important indicator of disease progression, should be further studied.
objectivesIn our study, we found that in the early stages of acute tendon injury, increased IL-1β can induce NETosis in neutrophils. Neutrophils and macrophages are early infiltrating cells in acute tendon injury, and their relationship has aroused our curiosity.
methodsIn our study, we used techniques such as high-throughput sequencing, tissue transmission electron microscopy, cell scanning electron microscopy, and multi-label immunofluorescence staining co-localization.
resultsWe found that as inflammation progresses, NETs secreted by neutrophils can induce macrophage pyroptosis by promoting the activation of AIM2. The pyroptosis macrophages can promote abnormal differentiation of tendon stem cells, thereby promoting the formation of tHO. To find an effective solution, we creatively combined different chiral lysines with bacterial cellulose and successfully prevented the formation of tHO.
conclusionOur research not only reveals from a new perspective that the IL-1β-NETs-AIM2 axis participates in the formation of tHO by orchestrating crosstalk between neutrophils and macrophages, but also provides a novel approach for the future clinical treatment of tHO.
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.