Evidence map›Paper›PMID 33144900›Full record

ArticlePain research & management2020

OPN Deficiency Increases the Severity of Osteoarthritis Associated with Aberrant Chondrocyte Senescence and Apoptosis and Upregulates the Expression of Osteoarthritis-Associated Genes.

Jian Tian, Chao Cheng, Shi-Da Kuang, Chao Su, Xin Zhao, Yi-Lin Xiong, Yu-Sheng Li, Shu-Guang Gao

Open access · goldAbstract read
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Article in Pain research & management, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

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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 2 institutions in 1 country.

Jian TianDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha 410008, Hunan, China.
Chao ChengDepartment of Orthopaedics, Yiyang Central Hospital, 118 North KangFu Road, Yiyang, Hunan 413000, China.
Shi-Da KuangDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha 410008, Hunan, China.
Chao SuDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha 410008, Hunan, China.
Xin ZhaoDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha 410008, Hunan, China.
Yi-Lin XiongDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha 410008, Hunan, China.
Yu-Sheng LiDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha 410008, Hunan, China.
Shu-Guang GaoDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha 410008, Hunan, China.ORCID 0000-0003-1135-7876
Central South University · CNYichang Central People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: A recent work has reported that the elevated osteopontin (OPN) levels in the articular cartilage and synovial fluid are correlated with the progressive osteoarthritis (OA) joint damage, and OPN has a protective effect against OA by suppressing the expressions of OA-associated genes. The present study examined whether the OPN deficiency was susceptible to OA through the regulation of chondrocyte senescence and apoptosis and the expressions of OA-associated genes. Methods: The mRNA levels of COL2A1 and OPN were compared between human OA chondrocytes and normal chondrocytes. The effects of OPN siRNA on the SA- Results: The mRNA levels of COL2A1 and OPN were decreased in knee OA chondrocytes in comparison with those in normal chondrocytes. The OPN deficiency enhanced the senescence and apoptosis of OA chondrocytes and increased the expressions of COL10A1, IL-1 Conclusions: The findings of this study suggest that the OPN deficiency can result in accelerated OA, which is associated with enhanced senescence and apoptosis of OA chondrocytes and the upregulated expressions of OA-associated genes.

Indexed as

Severity of Illness IndexAdolescentAdultAgedAnimalsApoptosisCartilage, ArticularCellular SenescenceChondrocytesFemaleGene ExpressionHumansInterleukin-1betaMaleMatrix Metalloproteinase 13Middle AgedIL1B protein, humanInterleukin-1betaMatrix Metalloproteinase 13MMP13 protein, humanOsteopontinSPP1 protein, human

Identifiers

PMID33144900
PMCPMC7599390
OpenAlexW3094299508

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.