Evidence map›Paper›PMID 34426599›Full record

ArticleScientific reports2021

LOXL2 attenuates osteoarthritis through inactivating Integrin/FAK signaling.

Caixia Zhang, Mengjiao Zhu, Huijuan Wang, Juan Wen, Ziwei Huang, Sheng Chen, Hongting Zhao, Huang Li

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. LOXL2 alleviates post-traumatic knee osteoarthritis and pain.Journal of orthopaedic translation · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. The Mechanism by WhichJournal of inflammation research · 2024
    Article
  10. Review
  11. Review
  12. 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

8 authors at 3 institutions in 1 country.

Caixia Zhang *Department of Orthodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, China.
Mengjiao Zhu *Shanghai Xuhui District Dental Center, 500 Fenglin Road, Shanghai, China.
Huijuan WangDepartment of Orthodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, China.
Juan WenDepartment of Orthodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, China.
Ziwei HuangDepartment of Orthodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, China.
Sheng ChenDepartment of Oral Pathology, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, China.
Hongting ZhaoMedical School of Nanjing University, Nanjing, China.
Huang LiDepartment of Orthodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, China. lihuang76@nju.edu.cn.
Nanjing University · CNNanjing Medical University · CNShanghai Xuhui Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Temporomandibular joint OA (TMJOA) is a common degenerative joint disease, leads to structural damage and ultimately loss of function. Matrix degradation is one of the first pathogenesis during the progression of OA, it was effective to inhibit matrix degradation to block the development of OA. In this study, an in vivo model (compressive mechanical force) and an in vitro model (IL-1β) were used to induce OA-like changes in TMJ cartilage and chondrocytes. We revealed lysyl oxidase like-2 (LOXL2) play a critical role in TMJOA. LOXL2 expression decreased in mechanical stress/IL-β induced TMJOA-like lesions in both in vivo models and in vitro models. Furthermore, recombinant LOXL2 (rhLOXL2) treatment ameliorated the degenerative changes induced by mechanical stress in vivo, including the thinning cartilage, down-expression of collagen II and proteoglycan, and over-expression of TNF-a, while LOXL2 antibody (anti-LOXL2) treatment exacerbated these changes. Mechanistically, the protection of LOXL2 in chondrocytes was induced partly through activation of the Integrin/FAK pathway. The inhibition of the Integrin/FAK pathway could neutralized the effects caused by rhLOXL2. Collectively, our study suggests that the LOXL2 plays a protective role in mechanical stress induced TMJOA-like changes, and the Integrin/FAK pathway may be a key downstream pathway in this process.

Indexed as

Signal TransductionAmino Acid OxidoreductasesAnimalsBiomechanical PhenomenaCartilageChondrocytesCollagen Type IIDown-RegulationExtracellular MatrixFocal Adhesion Protein-Tyrosine KinasesInflammationIntegrinsInterleukin-1betaMaleMandibleOsteoarthritisAmino Acid OxidoreductasesCollagen Type IIFocal Adhesion Protein-Tyrosine KinasesIntegrinsInterleukin-1betaTumor Necrosis Factor-alpha

Identifiers

PMID34426599
PMCPMC8382747
OpenAlexW3194860406

What OpenQuestion holds

Textmetadata
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.