Evidence map›Paper›PMID 33558275›Full record

ArticleJournal of investigative medicine : the official publication of the American Federation for Clinical Research2021

Mechanism of miR-218-5p in autophagy, apoptosis and oxidative stress in rheumatoid arthritis synovial fibroblasts is mediated by KLF9 and JAK/STAT3 pathways.

Ming Chen, Minghui Li, Na Zhang, Wenwen Sun, Hui Wang, Wei Wei

Open access · hybridAbstract read
In one paragraph

Article in Journal of investigative medicine : the official publication of the American Federation for Clinical Research, 2021. 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
2.5field-weighted citation impact, top 9% 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, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. KLF transcription factors in bone diseases.Journal of cellular and molecular medicine · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Rheumatoid Arthritis and Reactive Oxygen Species: A Review.Current issues in molecular biology · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. 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.

Ming ChenImmunology and Rheumatology Department, Tianjin Medical University General Hospital, Tianjin, China.
Minghui LiImmunology and Rheumatology Department, Tianjin Medical University General Hospital, Tianjin, China.
Na ZhangImmunology and Rheumatology Department, Tianjin Medical University General Hospital, Tianjin, China.
Wenwen SunImmunology and Rheumatology Department, Tianjin Medical University General Hospital, Tianjin, China.
Hui WangImmunology and Rheumatology Department, Tianjin Medical University General Hospital, Tianjin, China.
Wei WeiImmunology and Rheumatology Department, Tianjin Medical University General Hospital, Tianjin, China Weiwei1964@126-web.net.ORCID 0000-0002-9948-9613
Tianjin Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study was aimed to investigate the effects of miR-218-5p on the proliferation, apoptosis, autophagy, and oxidative stress of rheumatoid arthritis synovial fibroblasts (RASFs), and the related mechanisms. Quantitative reverse transcription-PCR showed that the expression of miR-218-5p in rheumatoid arthritis synovial tissue was significantly higher than that in healthy synovial tissue. Compared with healthy synovial fibroblasts, miR-218-5p expression was obviously upregulated in RASFs, while KLF9 protein expression was markedly downregulated. Mechanistically, miR-218-5p could directly bind to the 3' untranslated region of KLF9 to inhibit the expression of KLF9. Additionally, transfection of miR-218-5p small interfering RNA (siRNA) inhibited the proliferation but promoted apoptosis and autophagy of RASFs. Simultaneously, miR-218-5p silencing reduced reactive oxygen species and malondialdehyde levels and increased superoxide dismutase and glutathione peroxidase activity to improve oxidative stress in RASFs. More importantly, the introduction of KLF9 siRNA reversed the effects of miR-218-5p siRNA transfection on RASF proliferation, apoptosis, autophagy, and oxidative stress. What is more, silencing miR-218-5p inhibited the activation of JAK2/STAT3 signaling pathway by targeting KLF9. Collectively, knockdown of miR-218-5p could regulate the proliferation, apoptosis, autophagy and oxidative stress of RASFs by increasing the expression of KLF9 and inhibiting the activation of the JAK2/STAT3 signaling pathway, which may provide a potential target for the mechanism research of RA.

Indexed as

apoptosis

Identifiers

PMID33558275
PMCPMC8020083
OpenAlexW3128235130

What OpenQuestion holds

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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.