Evidence map›Paper›PMID 24691715›Full record

ArticleMolecular medicine reports2014

Autophagy in human articular chondrocytes is cytoprotective following glucocorticoid stimulation.

Ning Liu, Wenbo Wang, Zhe Zhao, Tao Zhang, Yuwen Song

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2014. 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
3.4field-weighted citation impact, top 8% 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, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Chondrotoxicity of Intra-Articular Injection Treatment: A Scoping Review.International journal of molecular sciences · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Monosodium Urate Crystal-Induced Chondrocyte Death via Autophagic Process.International journal of molecular sciences · 2015
    Article
  18. Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis.International journal of molecular sciences · 2015
    Review
  19. Review
  20. Review
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

5 authors at 2 institutions in 1 country.

Ning LiuDepartment of Orthopaedic Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Wenbo WangDepartment of Orthopaedic Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Zhe ZhaoDepartment of Orthopaedic Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Tao ZhangDepartment of Orthopaedic Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Yuwen SongDepartment of Orthopaedic Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
First Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

For the past 60 years, glucocorticosteroid (GC) drugs, including prednisone and dexamethasone (Dex), have been used for the treatment of early stage osteoarthritis (OA). However, multiple administration of GCs may destroy the articular cartilage. It has been previously reported that GC treatment may also lead to the initiation of autophagy, which is an essential mechanism for cell homeostasis and survival. Rapamycin (Rapa), an inhibitor of the mammalian target of Rapamycin, may cause a degeneration-associated pathology in organs and induce autophagy in a variety of cell types, which has been applied in the treatment of experimental OA. A previous study by our group observed that GC apparently increases the apoptosis of chondrocytes, resulting in the inhibition of extracellular matrix synthesis. Therefore, the present study aimed to further examine the effects of autophagy in chondrocytes under GC treatment and to verify the molecular mechanisms involved in the cytoprotective role of Rapa. Short-term GC treatment did not significantly inhibit chondrocyte viability, while cell autophagy was increased. In addition, upregulation of autophagy by Rapa prevented the expression of apoptosis-associated genes and improved cell activity. In conclusion, the present study revealed that increased autophagy is an adaptive response to protect chondrocytes from short‑term GC exposure, whereas prolonged GC treatment decreases autophagy and increases apoptosis in vitro. Upregulation of autophagy by Rapa may protect chondrocytes against the adverse effect induced by GC.

Indexed as

CytoprotectionApoptosisAutophagyCartilage, ArticularCells, CulturedCell SurvivalChondrocytesGlucocorticoidsHumansSirolimusGlucocorticoidsSirolimus

Identifiers

PMID24691715
PMCPMC4055442
OpenAlexW2093562680

What OpenQuestion holds

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LicenceCC BY
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.