Evidence map›Paper›PMID 37508475›Full record

ArticleCells2023

Cell Transitions Contribute to Glucocorticoid-Induced Bone Loss.

Xiaojing Qiao, Xiuju Wu, Yan Zhao, Yang Yang, Li Zhang, Xinjiang Cai, Jocelyn A Ma, Jaden Ji, Karen Lyons, Kristina I Boström and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Osteocytes Produces RANKL Via Wnt-TGFβ Signaling Axis for Osteoclastogenesis.International journal of biological sciences · 2025
    Article
  4. 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 at 1 institution in 1 country.

Xiaojing QiaoDivision of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
Xiuju WuDivision of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.ORCID 0000-0002-7499-0137
Yan ZhaoDivision of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
Yang YangDivision of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
Li ZhangDivision of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.ORCID 0000-0003-2638-2919
Xinjiang CaiDivision of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.ORCID 0000-0001-8933-7133
Jocelyn A MaDivision of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
Jaden JiDivision of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
Karen LyonsDepartment of Molecular, Cell & Developmental Biology at UCLA, Los Angeles, CA 90095, USA.
Kristina I BoströmDivision of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
Yucheng YaoDivision of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
University of California, Los Angeles · US

Funding

Molecular Mechanisms of MGP; Role in AVMsR01HL081397 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BOSTROM, KRISTINA I · 2006 to 2025
$7.7M
BMP and Notch Crosstalk in Cerebral Arteriovenous MalformationsR01NS079353 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Yucheng Yao · 2012 to 2026
$5.3M
Switch of Osteogenesis in Vascular CalcificationR01HL139675 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Yucheng Yao · 2018 to 2026
$3.6M
Endothelial Regulation of Vascular CalcificationR01HL158053 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BOSTROM, KRISTINA I · 2022 to 2025
$2.2M
Erasing ill features of arterial endothelial cells in hereditary hemorrhagic telangiectasiaR01HL162643 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YAO, YUCHENG · 2022 to 2025
$1.6M
NHLBI NIH HHS R01 HL081397NHLBI NIH HHS R01 HL139675NHLBI NIH HHS R01 HL158053NHLBI NIH HHS R01 HL162643NINDS NIH HHS NS79353NINDS NIH HHS R01 NS079353
6 · The paper itself

Abstract

Glucocorticoid-induced bone loss is a toxic effect of long-term therapy with glucocorticoids resulting in a significant increase in the risk of fracture. Here, we find that glucocorticoids reciprocally convert osteoblast-lineage cells into endothelial-like cells. This is confirmed by lineage tracing showing the induction of endothelial markers in osteoblast-lineage cells following glucocorticoid treatment. Functional studies show that osteoblast-lineage cells isolated from glucocorticoid-treated mice lose their capacity for bone formation but simultaneously improve vascular repair. We find that the glucocorticoid receptor directly targets Foxc2 and Osterix, and the modulations of Foxc2 and Osterix drive the transition of osteoblast-lineage cells to endothelial-like cells. Together, the results suggest that glucocorticoids suppress osteogenic capacity and cause bone loss at least in part through previously unrecognized osteoblast-endothelial transitions.

Indexed as

Bone Diseases, MetabolicGlucocorticoidsAnimalsMiceOsteoblastsOsteogenesisGlucocorticoidsbone lossendothelial-like cellsglucocorticoidosteoblasttransition

Identifiers

PMID37508475
PMCPMC10377921
OpenAlexW4383819274

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.