Evidence map›Paper›PMID 34847835›Full record

ArticleBioengineered2022

Ubiquitin-specific protease 3 attenuates interleukin-1β-mediated chondrocyte senescence by deacetylating forkhead box O-3 via sirtuin-3.

Qi Zhou, Wei Wang, Jun Wu, Shang Qiu, Shuai Yuan, Pei-Liang Fu, Qi-Rong Qian, Yao-Zeng Xu

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  5. Forkhead box O proteins in chondrocyte aging and diseases.Journal of orthopaedic translation · 2025
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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 1 country.

Qi ZhouDepartment of Orthopedics, The First Affiliated Hospital of Soochow University, Suzhou PR China.
Wei WangDepartment of Orthopedics, Changzheng Hospital, Naval Medical University, Shanghai PR China.
Jun WuDepartment of Orthopedics, Changzheng Hospital, Naval Medical University, Shanghai PR China.
Shang QiuDepartment of Orthopedics, The Affiliated Hospital of Xuzhou Medical University, Xuzhou Jiangsu, PR China.
Shuai YuanDepartment of Orthopedics, Changzheng Hospital, Naval Medical University, Shanghai PR China.
Pei-Liang FuDepartment of Orthopedics, Changzheng Hospital, Naval Medical University, Shanghai PR China.
Qi-Rong QianDepartment of Orthopedics, Changzheng Hospital, Naval Medical University, Shanghai PR China.
Yao-Zeng XuDepartment of Orthopedics, The First Affiliated Hospital of Soochow University, Suzhou PR China.
Shanghai Changzheng Hospital · CNFirst Affiliated Hospital of Soochow University · CNXuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA) affects approximately 12% of the aging Western population. The sirtuin/forkhead box O (SIRT/FOXO) signaling pathway plays essential roles in various biological processes. Despite it has been demonstrated that ubiquitin-specific protease 3 (USP3) inhibits chondrocyte apoptosis induced by interleukin (IL)-1β, the role of USP3/SIRT3/FOXO3 in the senescence of chondrocytes in OA is unclear. This study initially isolated articular chondrocytes and investigated the role of USP3 in IL-1β-induced senescence of chondrocytes. After USP3 was overexpressed or silenced by lentivirus, expressions of genes and proteins were detected using quantitative polymerase chain reaction and immunoblotting, respectively. Cell cycle analysis was performed using flow cytometry. Reactive oxygen species (ROS) levels and senescence were analyzed. Then, SIRT3 was inhibited or overexpressed to explore the underlying mechanism. We found that overexpression of USP3 hindered IL-1β-mediated cell cycle arrest, ROS generation, and chondrocyte senescence. The inhibition of SIRT3 blocked the protective effect of USP3 on cell senescence, whereas the overexpression of SIRT3 abolished USP3-silencing-induced cell senescence. Furthermore, SIRT3 attenuated cell senescence, probably by deacetylating FOXO3. USP3 upregulated SIRT3 to deacetylate FOXO3 and attenuated IL-1β-induced chondrocyte senescence. This study demonstrated that USP3 probably attenuated IL-1β-mediated chondrocyte senescence by deacetylating FOXO3 via SIRT3.

Indexed as

Cellular SenescenceAcetylationAnimalsChondrocytesForkhead Box Protein O3Interleukin-1betaOsteoarthritisRatsRats, Sprague-DawleySirtuin 1Ubiquitin-Specific ProteasesForkhead Box Protein O3FOXO3 protein, ratIL1B protein, ratInterleukin-1betaSirt1 protein, ratSirtuin 1Ubiquitin-Specific ProteasesUsp3 protein, ratdeacetylationFOXO3OsteoarthritissenescenceSIRT3ubiquitination

Identifiers

PMID34847835
PMCPMC8974216
OpenAlexW3215475567

What OpenQuestion holds

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LicenceCC BY
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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.