Evidence map›Paper›PMID 35851577›Full record

ArticleBone research2022

Osteocytes regulate bone anabolic response to mechanical loading in male mice via activation of integrin α5.

Dezhi Zhao, Rui Hua, Manuel A Riquelme, Hongyun Cheng, Teja Guda, Huiyun Xu, Sumin Gu, Jean X Jiang

Open access · goldAbstract read
In one paragraph

Article in Bone research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 31 citations in OpenAlex.

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  12. Role and mechanism of Integrin α5β1 in bone formation and disease.Frontiers in cell and developmental biology · 2025
    Review
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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 2 countries.

Dezhi ZhaoDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX, USA.
Rui HuaDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX, USA.
Manuel A RiquelmeDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX, USA.
Hongyun ChengDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX, USA.
Teja GudaDepartment of Biomedical Engineering and Chemical Engineering, University of Texas, San Antonio, TX, USA.
Huiyun XuSchool of Life Sciences, Northwestern Polytechnical University, Xi'an, China.ORCID http://orcid.org/0000-0002-3037-0358
Sumin GuDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX, USA.
Jean X JiangDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX, USA. jiangj@uthscsa.edu.ORCID http://orcid.org/0000-0002-2185-5716
The University of Texas Health Science Center at San Antonio · USNorthwestern Polytechnical University · CNThe University of Texas at San Antonio · US

Funding

Connexin channels in transducing mechanical signals in boneR01AR072020 · NIAMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI JIANG, JEAN X · 2018 to 2022
$1.7M
NIAMS NIH HHS R01 AR072020U.S. Department of Health & Human Services | NIH | Office of Extramural Research, National Institutes of Health (OER) AR072020Welch Foundation AQ-1507
6 · The paper itself

Abstract

Physical mechanical stimulation can maintain and even increase bone mass. Here, we report an important role of osteocytic integrin α5 in regulating the anabolic response of bone to mechanical loading using an Itga5 conditional gene knockout (cKO) mouse model. Integrin α5 gene deletion increased apoptotic osteocytes and reduced cortical anabolic responses to tibial compression including decreased endosteal osteoblasts and bone formation, and increased endosteal osteoclasts and bone resorption, contributing to the decreased bone area fraction and biomechanical properties, leading to an enlarged bone marrow area in cKO mice. Similar disruption of anabolic responses to mechanical loading was also detected in cKO trabecular bone. Moreover, integrin α5 deficiency impeded load-induced Cx43 hemichannel opening, and production and release of PGE2, an anabolic factor, resulting in attenuated effects of the loading on catabolic sclerostin (SOST) reduction and anabolic β-catenin increase. Together, this study shows an indispensable role of integrin α5 in osteocytes in the anabolic action of mechanical loading on skeletal tissue through activation of hemichannels and PGE2-evoked gene expression. Integrin α5 could act as a potential new therapeutic target for bone loss, especially in the elderly population with impeded mechanical sensitivity.

Identifiers

PMID35851577
PMCPMC9293884
OpenAlexW4285729356

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.