Evidence map›Paper›PMID 39406726›Full record

ArticleBone research2024

Periostin

Ziyan Wang, Minmin Lin, Yonghao Pan, Yang Liu, Chengyu Yang, Jianqun Wu, Yan Wang, Bingtong Yan, Jingjing Zhou, Rouxi Chen and 1 more

Abstract read
In one paragraph

Article in Bone research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Hierarchical Targeting of TREM2Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
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

11 authors.

Ziyan WangDepartment of Biomedical Engineering, Southern University of Science and Technology, Shenzhen, Guangdong, 518055, China.ORCID http://orcid.org/0000-0001-8158-1828
Minmin LinDepartment of Biomedical Engineering, Southern University of Science and Technology, Shenzhen, Guangdong, 518055, China.
Yonghao PanDepartment of Biomedical Engineering, Southern University of Science and Technology, Shenzhen, Guangdong, 518055, China.
Yang LiuDepartment of Biomedical Engineering, Southern University of Science and Technology, Shenzhen, Guangdong, 518055, China.
Chengyu YangDepartment of Biomedical Engineering, Southern University of Science and Technology, Shenzhen, Guangdong, 518055, China.
Jianqun WuDepartment of Biomedical Engineering, Southern University of Science and Technology, Shenzhen, Guangdong, 518055, China.
Yan WangDepartment of Biomedical Engineering, Southern University of Science and Technology, Shenzhen, Guangdong, 518055, China.
Bingtong YanDepartment of Biomedical Engineering, Southern University of Science and Technology, Shenzhen, Guangdong, 518055, China.
Jingjing ZhouDepartment of Biomedical Engineering, Southern University of Science and Technology, Shenzhen, Guangdong, 518055, China.
Rouxi ChenDepartment of Materials Science and Engineering, Southern University of Science and Technology, Shenzhen, Guangdong, 518055, China.
Chao LiuDepartment of Biomedical Engineering, Southern University of Science and Technology, Shenzhen, Guangdong, 518055, China. liuc33@sustech.edu.cn.ORCID http://orcid.org/0000-0001-6637-1689

Funding

Shenzhen Science and Technology Innovation Commission JCYJ20190809114209434Shenzhen Science and Technology Innovation Commission KQTD20200820113012029
6 · The paper itself

Abstract

Myeloid cells are pivotal in the inflammatory and remodeling phases of fracture repair. Here, we investigate the effect of periostin expressed by myeloid cells on bone regeneration in a monocortical tibial defect (MTD) model. In this study, we show that periostin is expressed by periosteal myeloid cells, primarily the M2 macrophages during bone regeneration. Knockout of periostin in myeloid cells reduces cortical bone thickness, disrupts trabecular bone connectivity, impairs repair impairment, and hinders M2 macrophage polarization. Mechanical stimulation is a regulator of periostin in macrophages. By activating transforming growth factor-β (TGF-β), it increases periostin expression in macrophages and induces M2 polarization. This mechanosensitive effect also reverses the delayed bone repair induced by periostin deficiency in myeloid cells by strengthening the angiogenesis-osteogenesis coupling. In addition, transplantation of mechanically conditioned macrophages into the periosteum over a bone defect results in substantially enhanced repair, confirming the critical role of macrophage-secreted periostin in bone repair. In summary, our findings suggest that mechanical stimulation regulates periostin expression and promotes M2 macrophage polarization, highlighting the potential of mechanically conditioned macrophages as a therapeutic strategy for enhancing bone repair.

Indexed as

Bone RegenerationCell Adhesion MoleculesMacrophagesMyeloid CellsAnimalsMechanotransduction, CellularMiceMice, Inbred C57BLMice, KnockoutOsteogenesisPeriostinCell Adhesion MoleculesPeriostinPostn protein, mouse

Identifiers

PMID39406726
PMCPMC11480347

What OpenQuestion holds

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LicenceCC BY
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 OpenQuestion graph.