Evidence map›Paper›PMID 31737959›Full record

ArticleCell proliferation2020

Inhibition of Ctsk modulates periodontitis with arthritis via downregulation of TLR9 and autophagy.

Wei Wei, Jie Ren, Wuwei Yin, Handong Ding, Qiuyu Lu, Liangyu Tan, Shibing Deng, Jie Liu, Qin Yang, Jiajia Wang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Cathepsin KFrontiers in cell and developmental biology · 2022
    Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. [Mechanism and material basis ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Article
  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

13 authors at 1 institution in 1 country.

Wei WeiThe State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Jie RenThe State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Wuwei YinThe State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Handong DingThe State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Qiuyu LuThe State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Liangyu TanThe State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Shibing DengThe State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Jie LiuThe State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Qin YangThe State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Jiajia WangThe State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Min WangThe State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Yuan YueThe State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, China.
Liang HaoThe State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Sichuan, China.ORCID https://orcid.org/0000-0001-7207-9131
Sichuan University · CN

Funding

National Natural Science Foundation of China 81400523National Natural Science Foundation of China 81570987National Natural Science Foundation of China 81601909Sichuan Provincial Science and Technology Foundation 2018FZ0027Sichuan Provincial Science and Technology Foundation 2018FZ0042Sichuan Provincial Science and Technology Foundation 2019YFS0359
6 · The paper itself

Abstract

objectivesThe mechanisms underlying the effects of Toll-like receptor 9 (TLR9) and autophagy on rheumatoid arthritis (RA)-aggravated periodontitis are unclear. We aimed to explore a novel target, cathepsin K (Ctsk)-mediated TLR9-related autophagy, during the progress of periodontitis with RA. MATERIALS AND

methodsDBA/J1 mouse model of periodontitis with RA was created by local colonization of Porphyromonas gingivalis (Pg) and injection of collagen. The expression of Ctsk was inhibited by adeno-associated virus (AAV). Micro-CT, immunohistochemistry (IHC), Western blot and quantitative real-time polymerase chain reaction (qRT-PCR) were used to detect the expression of TLR9-related autophagy in periodontitis with RA. Small interfering RNA (siRNA) and CpG oligodeoxynucleotides (CpG ODN) were applied in macrophages. Western blot, immunofluorescence (IF) and qRT-PCR were used to verify the in vivo results.

resultsRA can promote periodontitis bone destruction in the lesion area, while inhibiting Ctsk could effectively alleviate this effect. The infiltration of macrophages, TLR9, autophagy proteins (TFEB and LC3) and inflammatory cytokines increased in the periodontitis-with-RA group and was reduced by the inhibition of Ctsk in the periodontal region. Macrophage stimulation confirmed the in vivo results. With the activation of TLR9 by CpG ODN, inhibition of Ctsk could suppress both TLR9 downstream signalling proteins and autophagy-related proteins.

conclusionsThis study advanced a novel role for Ctsk in TLR9 and autophagy to explain the interaction between periodontitis and RA.

Indexed as

AnimalsArthritis, RheumatoidBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCathepsin KDisease Models, AnimalDown-RegulationMaleMiceMice, Inbred DBAMicrotubule-Associated ProteinsOligodeoxyribonucleotidesPeriodontitisToll-Like Receptor 9Basic Helix-Loop-Helix Leucine Zipper Transcription FactorsCathepsin KCPG-oligonucleotideCtsk protein, mouseMap1lc3b protein, mouseMicrotubule-Associated ProteinsOligodeoxyribonucleotidesTcfeb protein, mouseTlr9 protein, mouseToll-Like Receptor 9arthritisautophagycathepsin KperiodontitisToll-like receptor 9

Identifiers

PMID31737959
PMCPMC6985664
OpenAlexW2986883131

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.