Evidence map›Paper›PMID 31922219›Full record

ArticleInternational journal of molecular medicine2020

The GSK‑3β/β‑catenin signaling pathway is involved in HMGB1‑induced chondrocyte apoptosis and cartilage matrix degradation.

Zhiyong Shu, Xiaogang Miao, Tainhua Tang, Peng Zhan, Langqing Zeng, Yuwen Jiang

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  4. Flavonoids ofPreventive nutrition and food science · 2026
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  7. Review
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  13. Article
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  16. [Mechanism of high expression of high mobility group protein 1 in a rat model of knee osteoarthritis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Article
  17. Article
  18. Article
  19. 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

6 authors at 1 institution in 1 country.

Zhiyong ShuDepartment of Orthopedics, Zhuhai People's Hospital, Zhuhai, Guangdong 519000, P.R. China.
Xiaogang MiaoDepartment of Orthopedics, Zhuhai People's Hospital, Zhuhai, Guangdong 519000, P.R. China.
Tainhua TangDepartment of Orthopedics, Zhuhai People's Hospital, Zhuhai, Guangdong 519000, P.R. China.
Peng ZhanDepartment of Orthopedics, Zhuhai People's Hospital, Zhuhai, Guangdong 519000, P.R. China.
Langqing ZengDepartment of Orthopedics, Zhuhai People's Hospital, Zhuhai, Guangdong 519000, P.R. China.
Yuwen JiangDepartment of Orthopedics, Zhuhai People's Hospital, Zhuhai, Guangdong 519000, P.R. China.
Zhuhai People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Knee osteoarthritis (KOA) is a common joint disease with a high incidence rate among middle‑aged and elderly individuals. However, the precise underlying pathological mechanisms and effective treatment of this disease remain to be determined. To explore the effect of high mobility group box 1 (HMGB1) on chondrocyte apoptosis and catabolism, the ATDC5 cell line was cultured as an in vitro model for cartilage research. Cultured cells were treated with recombinant HMGB1 at different concentrations. Hoechst staining and flow cytometry demonstrated that HMGB1 administration significantly induced apoptosis of ATDC5 cells, which was the same as the effect of interleukin‑1β treatment. HMGB1 also induced cartilage matrix degradation, as shown by Alcian blue staining. Moreover, HMGB1 markedly upregulated the expression levels of matrix metallopeptidases (MMPs) and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS), while genetic silencing of HMGB1 significantly suppressed their expressions. The glycogen synthase kinase (GSK)‑3β/β‑catenin pathway was activated upon HMGB1 treatment. Pharmacological inhibitors or HMGB1 knockdown inactivated the GSK‑3β/β‑catenin pathway, inhibited the expression levels of downstream genes, including MMPs and ADAMTS, and attenuated the apoptosis of ATDC5 cells. Furthermore, the data demonstrated that HMGB1 promoted chondrocyte dysfunction via the regulation of estrogen sulfotransferase and Runt‑related transcription factor 2. Thus, the findings of the present study demonstrated that HMGB1 induces chondrocyte cell apoptosis via activation of GSK‑3β/β‑catenin and the subsequent expression of multiple targeted genes.

Indexed as

AnimalsApoptosisbeta CateninCartilageChondrocytesGlycogen Synthase Kinase 3 betaHMGB1 ProteinMatrix MetalloproteinasesMiceSignal Transductionbeta CateninCTNNB1 protein, mouseGlycogen Synthase Kinase 3 betaGsk3b protein, mouseHMGB1 ProteinHMGB1 protein, mouseMatrix Metalloproteinases

Identifiers

PMID31922219
PMCPMC7015138
OpenAlexW3000558321

What Socratic holds

Textmetadata
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 Socratic graph.