Evidence map›Paper›PMID 35005113›Full record

ArticleGenes & diseases2022

Osteopontin inhibits osteoarthritis progression via the OPN/CD44/PI3K signal axis.

Qing Liu, Hao Zeng, Yuhao Yuan, Zhiwei Wang, Ziyi Wu, Wei Luo

Open access · diamondAbstract read
In one paragraph

Article in Genes & diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

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  11. [FJX1 overexpression is associated with poor prognosis and promotes gastric cancer proliferationNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
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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

6 authors at 1 institution in 2 countries.

Qing LiuDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87th Xiangya Road, Changsha, Hunan 410008, PR China.
Hao ZengDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87th Xiangya Road, Changsha, Hunan 410008, PR China.
Yuhao YuanDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87th Xiangya Road, Changsha, Hunan 410008, PR China.
Zhiwei WangDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87th Xiangya Road, Changsha, Hunan 410008, PR China.
Ziyi WuDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87th Xiangya Road, Changsha, Hunan 410008, PR China.
Wei LuoDepartment of Orthopaedics, Xiangya Hospital, Central South University, 87th Xiangya Road, Changsha, Hunan 410008, PR China.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chondrocyte degeneration and extracellular matrix component loss are the primary causes of osteoarthritis (OA). OA can be treated by inhibiting chondrocyte degeneration and increasing extracellular matrix component secretion. Osteopontin (OPN), a multifunctional protein, has gained immense attention with regard to its involvement in OA. This study aimed to explore the therapeutic value and mechanism of action of OPN in OA treatment. Results of the histomorphological analysis revealed a worn-off OA cartilage tissue surface, cartilage matrix layer deterioration, and calcium salt deposition. Compared to that in normal chondrocytes, in OA chondrocytes, the OPN, CD44, and PI3K protein and mRNA expression was upregulated. Further, siOPN, rhOPN, and rhOPN plus LS-C179404 interfered with OA chondrocytes. As verified in mice, OPN directly inhibited the expression level of PI3K in OA chondrocytes by binding with CD44. Morphological analysis of the knee joints demonstrated that OPN effectively inhibited OA progression via the OPN/CD44/PI3K signal axis. In conclusion, OPN activates intracellular PI3K signaling molecules by binding to CD44 on the cell surface to cause downstream cascading effects, thereby delaying chondrocyte degeneration and reducing cartilage matrix component loss; therefore, OPN is a potential therapeutic agent for OA.

Indexed as

Cartilage degenerationCartilage matrixCD44OsteoarthritisOsteopontinPhosphatidylinositol-3-kinase

Identifiers

PMID35005113
PMCPMC8720673
OpenAlexW3037105462

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.