Evidence map›Paper›PMID 37115368›Full record

ArticleInflammation2023

Inhibition of NF-κB Signaling-Mediated Crosstalk Between Macrophages and Preosteoblasts by Metformin Alleviates Trauma-Induced Heterotopic Ossification.

Jia Hou, Jie Chen, Jingjing Fan, Zhimin Tang, Wenwen Zhou, Hui Lin

Abstract read
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In one paragraph

Article in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.7field-weighted citation impact, top 6% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Gut microbiome-dependent IL-1 signaling is a mediator of ACVR1bioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Fibroblasts in heterotopic ossification: mechanisms and therapeutic targets.International journal of biological sciences · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Jia Hou *Department of Pathophysiology, School of Basic Medical Sciences, Nanchang University, Nanchang, 330006, Jiangxi, China.
Jie Chen *Department of Pathophysiology, School of Basic Medical Sciences, Nanchang University, Nanchang, 330006, Jiangxi, China.
Jingjing FanDepartment of Pathophysiology, School of Basic Medical Sciences, Nanchang University, Nanchang, 330006, Jiangxi, China.
Zhimin TangDepartment of Pathophysiology, School of Basic Medical Sciences, Nanchang University, Nanchang, 330006, Jiangxi, China.
Wenwen ZhouDepartment of Pathophysiology, School of Basic Medical Sciences, Nanchang University, Nanchang, 330006, Jiangxi, China.
Hui LinDepartment of Pathophysiology, School of Basic Medical Sciences, Nanchang University, Nanchang, 330006, Jiangxi, China. huilin88@ncu.edu.cn.
Nanchang University · CN

Funding

National Natural Science Foundation of China 31900852Nature Science Foundation of Jiangxi Province 20181BAB215012; 20192ACB21026;20224ACB206024
6 · The paper itself

Abstract

Heterotopic ossification (HO) is a pathological condition that occurs in soft tissues following severe trauma. The exact pathogenesis of HO remains unclear. Studies have shown that inflammation predisposes patients to the development of HO and triggers ectopic bone formation. Macrophages are crucial mediators of inflammation and are involved in HO development. The present study investigated the inhibitory effect and underlying mechanism of metformin on macrophage infiltration and traumatic HO in mice. Our results found that abundant levels of macrophages were recruited to the injury site during early HO progression and that early administration of metformin prevented traumatic HO in mice. Furthermore, we found that metformin attenuated macrophage infiltration and the NF-κB signaling pathway in injured tissue. The monocyte-to-macrophage transition in vitro was suppressed by metformin and this event was mediated by AMPK. Finally, we showed that inflammatory mediator's regulation by macrophages targeted preosteoblasts, leading to elevated BMP signaling, and osteogenic differentiation and driving HO formation, and this effect was blocked after the activation of AMPK in macrophages. Collectively, our study suggests that metformin prevents traumatic HO by inhibiting of NF-κB signaling in macrophages and subsequently attenuating BMP signaling and osteogenic differentiation in preosteoblasts. Therefore, metformin may serve as a therapeutic drug for traumatic HO by targeting NF-κB signaling in macrophages.

Indexed as

MetforminOssification, HeterotopicAMP-Activated Protein KinasesAnimalsMacrophagesMiceNF-kappa BOsteogenesisSignal TransductionAMP-Activated Protein KinasesMetforminNF-kappa Bheterotopic ossificationmacrophagesmetforminNF-κB signaling

Identifiers

PMID37115368
OpenAlexW4367318308

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.