Evidence map›Paper›PMID 40730513›Full record

ArticleCell proliferation2026

Mechanism of ITGB2 in Osteoclast Differentiation in Osteoarthritis.

Yang Yang, Rui Sun, Zhibin Lan, Qi Ma, Gang Wu, Di Xue, Zhirong Chen, Yajing Su, Ye Ma, Xiaolei Chen and 7 more

Erratum issuedAbstract read
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In one paragraph

Article in Cell proliferation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors.

Yang YangThe Third Ward of Orthopaedic Department, Institute of Osteoarthropathy, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Rui SunThe Third Ward of Orthopaedic Department, Institute of Osteoarthropathy, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Zhibin LanThe Third Ward of Orthopaedic Department, Institute of Osteoarthropathy, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Qi MaThe Third Ward of Orthopaedic Department, Institute of Osteoarthropathy, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Gang WuThe Third Ward of Orthopaedic Department, Institute of Osteoarthropathy, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Di XueNingxia Key Laboratory of Clinical and Pathogenic Microbiology, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Zhirong ChenThe Third Ward of Orthopaedic Department, Institute of Osteoarthropathy, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Yajing SuNingxia Key Laboratory of Clinical and Pathogenic Microbiology, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Ye MaThe Third Ward of Orthopaedic Department, Institute of Osteoarthropathy, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Xiaolei ChenThe Third Ward of Orthopaedic Department, Institute of Osteoarthropathy, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Jiangbo YanThe Third Ward of Orthopaedic Department, Institute of Osteoarthropathy, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Long MaThe Third Ward of Orthopaedic Department, Institute of Osteoarthropathy, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Xiaoxin HeThe Third Ward of Orthopaedic Department, Institute of Osteoarthropathy, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Kuanmin TianThe Third Ward of Orthopaedic Department, Institute of Osteoarthropathy, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Xiaoyi MaThe Third Ward of Orthopaedic Department, Institute of Osteoarthropathy, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Xue LinNingxia Key Laboratory of Clinical and Pathogenic Microbiology, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.
Qunhua JinThe Third Ward of Orthopaedic Department, Institute of Osteoarthropathy, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, People's Republic of China.ORCID https://orcid.org/0009-0008-9392-9113

Funding

Autonomous Region Major Scientific and Technological Achievements Transformation Project 2023CJE09037Key R&D Project of Autonomous Region 2023BEG02018National Natural Science Foundation of China 82160433National Natural Science Foundation of China U22A20285Ningxia Medical University General Hospital "Medical Engineering Special" NYZYYG-001
6 · The paper itself

Abstract

Transcriptomics studies have identified integrin receptor β2 subunit (ITGB2) as a core gene in osteoarthritis (OA), strongly linked to osteoclast function in the subchondral bone. However, the mechanism through which ITGB2 regulates osteoclast function in OA remains unclear. In this study, we found that ITGB2 was negatively correlated with ITGB1 in the human subchondral bone. Proteomic analysis indicated that integrin binding is crucial in OA subchondral bone, with ITGB2 identified as a significantly upregulated protein in OA. In vitro experiments using immunoprecipitation and bimolecular fluorescence complementation revealed that ITGB2, but not ITGB1, directly interacts with Rac1 during osteoclast differentiation. Activated Rac1 promotes osteoclast differentiation and bone resorption through several mechanisms. ITGB2 knockdown reduced Rac1-GTP levels and increased ITGB1 expression. ITGB2 inhibition reduced actin ring formation and microtubule migration to the cell edge during osteoclast differentiation. Additionally, overexpression of ITGB1 in ITGB2-knockdown cells not only further suppressed ITGB2 expression but also exacerbated the inhibition of osteoclast differentiation. In a DMM mouse model, ITGB2 was associated with osteoclast activity in the subchondral bone. ITGB2 knockdown significantly reduced bone resorption and slowed OA progression by inhibiting osteoclastogenesis. In conclusion, our study identified a novel mechanism for the reciprocal regulation of integrin subunits. Moreover, inhibition of the ITGB2 signalling pathway slows subchondral bone remodelling in osteoarthritis by inhibiting osteoclast differentiation, offering a potential strategy for targeted therapeutic interventions.

Indexed as

CD18 AntigensCell DifferentiationOsteoarthritisOsteoclastsAnimalsBone ResorptionHumansIntegrin beta1MaleMiceMice, Inbred C57BLOsteogenesisrac1 GTP-Binding ProteinSignal TransductionCD18 AntigensIntegrin beta1rac1 GTP-Binding Proteinintegrinosteoarthritisosteoclast differentiationRac1subchondral bone

Identifiers

PMID40730513
PMCPMC12961538

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.