Evidence map›Paper›PMID 37887278›Full record

ArticleCells2023

Aurora Kinase A Regulates Cell Transitions in Glucocorticoid-Induced Bone Loss.

Xiaojing Qiao, Yang Yang, Yan Zhao, Xiuju Wu, Li Zhang, Xinjiang Cai, Jaden Ji, Kristina I Boström, Yucheng Yao

Open access · goldAbstract read
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. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 40% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

9 authors at 1 institution in 1 country.

Xiaojing QiaoDivision of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679, USA.
Yang YangDivision of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679, USA.
Yan ZhaoDivision of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679, USA.
Xiuju WuDivision of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679, USA.ORCID 0000-0002-7499-0137
Li ZhangDivision of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679, USA.
Xinjiang CaiDivision of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679, USA.ORCID 0000-0001-8933-7133
Jaden JiDivision of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679, USA.
Kristina I BoströmDivision of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679, USA.
Yucheng YaoDivision of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679, 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
Regulation of Vascular Calcification by Adventitial Endothelial CellsK08HL168147 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Xinjiang Cai · 2023 to 2026
$692k
NHLBI NIH HHS K08 HL168147NHLBI 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 severe and toxic effect of long-term therapy with glucocorticoids, which are currently prescribed for millions of people worldwide. Previous studies have uncovered that glucocorticoids reciprocally converted osteoblast lineage cells into endothelial-like cells to cause bone loss and showed that the modulations of Foxc2 and Osterix were the causative factors that drove this harmful transition of osteoblast lineage cells. Here, we find that the inhibition of aurora kinase A halts this transition and prevents glucocorticoid-induced bone loss. We find that aurora A interacts with the glucocorticoid receptor and show that this interaction is required for glucocorticoids to modulate Foxc2 and Osterix. Together, we identify a new potential approach to counteracting unwanted transitions of osteoblast lineage cells in glucocorticoid treatment and may provide a novel strategy for ameliorating glucocorticoid-induced bone loss.

Indexed as

Aurora Kinase ABone Diseases, MetabolicGlucocorticoidsAnimalsOsteoblastsReceptors, GlucocorticoidAurora Kinase AGlucocorticoidsReceptors, Glucocorticoidaurora kinasebone lossendothelial-like cellsglucocorticoidosteoblasttransition

Identifiers

PMID37887278
PMCPMC10605378
OpenAlexW4387529309

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.