Evidence map›Paper›PMID 39688917›Full record

ArticleJCI insight2024

Negative feedback between PTH1R and IGF1 through the Hedgehog pathway in mediating craniofacial bone remodeling.

Yi Fan, Ping Lyu, Jiahe Wang, Yali Wei, Zucen Li, Shiwen Zhang, Takehito Ouchi, Junjun Jing, Quan Yuan, Clifford J Rosen and 1 more

Abstract read
In one paragraph

Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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.

Yi FanState Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases.
Ping LyuState Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases.
Jiahe WangState Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases.
Yali WeiState Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases.
Zucen LiState Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases.
Shiwen ZhangState Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases.
Takehito OuchiDepartment of Physiology, Tokyo Dental College, Tokyo, Japan.
Junjun JingState Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases.
Quan YuanState Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases.
Clifford J RosenMaine Medical Center Research Institute, Scarborough, Maine, USA.
Chenchen ZhouState Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regeneration of orofacial bone defects caused by inflammation-related diseases or trauma remains an unmet challenge. Parathyroid hormone 1 receptor (PTH1R) signaling is a key mediator of bone remodeling whereas the regulatory mechanisms of PTH1R signaling in oral bone under homeostatic or inflammatory conditions have not been demonstrated by direct genetic evidence. Here, we observed that deletion of PTH1R in Gli1+ progenitors led to increased osteogenesis and osteoclastogenesis. Single-cell and bulk RNA-Seq analysis revealed that PTH1R suppressed the osteogenic potential of Gli1+ progenitors during inflammation. Moreover, we identified upregulated IGF1 expression upon PTH1R deletion. Dual deletion of IGF1 and PTH1R ameliorated the bone-remodeling phenotypes in PTH1R-deficient mice. Furthermore, in vivo evidence revealed an inverse relationship between PTH1R and Hedgehog signaling, which was responsible for the upregulated IGF1 production. Our work underscored the negative feedback between PTH1R and IGF1 in craniofacial bone turnover and revealed mechanisms modulating orofacial bone remodeling.

Indexed as

Bone RemodelingFacial BonesHedgehog ProteinsInsulin-Like Growth Factor IReceptor, Parathyroid Hormone, Type 1AnimalsFeedback, PhysiologicalMiceMice, KnockoutOsteogenesisSignal TransductionZinc Finger Protein GLI1Gli1 protein, mouseHedgehog Proteinsinsulin-like growth factor-1, mouseInsulin-Like Growth Factor IReceptor, Parathyroid Hormone, Type 1Zinc Finger Protein GLI1Bone biologyBone developmentDevelopmentG protein–coupled receptorsOsteoclast/osteoblast biology

Identifiers

PMID39688917
PMCPMC11948590

What Socratic 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 Socratic graph.