Evidence map›Paper›PMID 27117872›Full record

ArticleScientific reports2016

sFRP4-dependent Wnt signal modulation is critical for bone remodeling during postnatal development and age-related bone loss.

Ryuma Haraguchi, Riko Kitazawa, Kiyoshi Mori, Ryosuke Tachibana, Hiroshi Kiyonari, Yuuki Imai, Takaya Abe, Sohei Kitazawa

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 76 citations in OpenAlex.

  1. ROS Activated NETosis of Bone Marrow CD55Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  4. [Bisphosphonates-related osteonecrosis of the jaw: A case report].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2025
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  8. JBMR plus · 2024
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  12. Article
  13. Article
  14. Cellular senescence in skeletal disease: mechanisms and treatment.Cellular & molecular biology letters · 2023
    Review
  15. Article
  16. Review
  17. Article
  18. The role of wnt signaling in diabetes-induced osteoporosis.Diabetology & metabolic syndrome · 2023
    Review
  19. Article
  20. 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

8 authors at 3 institutions in 1 country.

Ryuma HaraguchiDepartment of Molecular Pathology, Ehime University Graduate School of Medicine, Shitsukawa, Toon City, Ehime 791-0295, Japan.
Riko KitazawaDepartment of Molecular Pathology, Ehime University Graduate School of Medicine, Shitsukawa, Toon City, Ehime 791-0295, Japan.
Kiyoshi MoriDepartment of Pathology, National Hospital Organization, Osaka National Hospital, Hoenzaka, Chuo-ku, Osaka City, Osaka 540-0006, Japan.
Ryosuke TachibanaDepartment of Molecular Pathology, Ehime University Graduate School of Medicine, Shitsukawa, Toon City, Ehime 791-0295, Japan.
Hiroshi KiyonariAnimal Resource Development Unit, RIKEN Center for Life Science Technologies, Minatojima Minami-machi, Chuo-Ku, Kobe City, Hyogo 650-0047, Japan.
Yuuki ImaiDivision of Integrative Pathophysiology, Proteo-Science Center, Ehime University Graduate School of Medicine, Shitsukawa, Toon City, Ehime 791-0295, Japan.
Takaya AbeAnimal Resource Development Unit, RIKEN Center for Life Science Technologies, Minatojima Minami-machi, Chuo-Ku, Kobe City, Hyogo 650-0047, Japan.
Sohei KitazawaDepartment of Molecular Pathology, Ehime University Graduate School of Medicine, Shitsukawa, Toon City, Ehime 791-0295, Japan.
Ehime University · JPEhime University Hospital · JPOsaka National Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

sFRP4 is an extracellular Wnt antagonist that fine-tunes its signal activity by direct binding to Wnts. Bone fragility under oxidative stress by diabetes and aging is partly related to the suppression of the Wnt signal through upregulated sFRP4. Here, to explore the functions of sFRP4 as a balancer molecule in bone development and remodeling, we analyzed the sFRP4 knock-in mouse strain. X-gal and immunohistochemically stained signals in sFRP4-LacZ heterozygous mice were detectable in restricted areas, mostly in osteoblasts and osteoclasts, of the femoral diaphysis after neonatal and postnatal stages. Histological and μCT analyses showed increased trabecular bone mass with alteration of the Wnt signal and osteogenic activity in sFRP4 mutants; this augmented the effect of the buildup of trabecular bone during the ageing period. Our results indicate that sFRP4 plays a critical role in bone development and remodeling by regulating osteoblasts and osteoclasts, and that its functional loss prevents age-related bone loss in the trabecular bone area. These findings imply that sFRP4 functions as a key potential endogenous balancer of the Wnt signaling pathway by efficiently having direct influence on both bone formation and bone absorption during skeletal bone development and maintenance through remodeling.

Indexed as

AnimalsBone RemodelingCancellous BoneDisease Models, AnimalGene Knock-In TechniquesMiceOsteoblastsOsteoclastsOsteoporosisProto-Oncogene ProteinsSecreted Frizzled-Related ProteinsWnt Signaling PathwayProto-Oncogene ProteinsSecreted Frizzled-Related ProteinsSfrp4 protein, mouse

Identifiers

PMID27117872
PMCPMC4846872
OpenAlexW2342999456

What OpenQuestion holds

Textmetadata
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.