Evidence map›Paper›PMID 30729704›Full record

ArticleJournal of cellular and molecular medicine2019

Chondroprotection of PPARα activation by WY14643 via autophagy involving Akt and ERK in LPS-treated mouse chondrocytes and osteoarthritis model.

Yang Zhou, Xiaolei Chen, Ning Qu, Bing Zhang, Chun Xia

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

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  7. Osteoarthritis: Role of Peroxisome Proliferator-Activated Receptors.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Review
  10. Upregulation of osteoprotegerin inhibitsExperimental and therapeutic medicine · 2022
    Article
  11. Article
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  13. Article
  14. Article
  15. Article
  16. Article
  17. Essential Roles of PPARs in Lipid Metabolism during Mycobacterial Infection.International journal of molecular sciences · 2021
    Review
  18. Article
  19. Review
  20. Oxidative medicine and cellular longevity · 2020
    Article
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.

Yang ZhouZhongshan Hospital, Xiamen University, Xiamen, Fujian, China.
Xiaolei ChenZhongshan Hospital, Xiamen University, Xiamen, Fujian, China.
Ning QuSchool of Medicine, Xiamen University, Xiamen, Fujian, China.
Bing ZhangSchool of Medicine, Xiamen University, Xiamen, Fujian, China.
Chun XiaZhongshan Hospital, Xiamen University, Xiamen, Fujian, China.ORCID 0000-0001-8585-9313
Zhongshan Hospital of Xiamen University · CNXiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy maintains cellular homoeostasis. The enhancement of autophagy in chondrocytes could prevent osteoarthritis (OA) progression in articular cartilage. Peroxisome proliferator-activated receptor α (PPARα) activation may also protect articular chondrocytes against cartilage degradation in OA. However, whether the protective effect of activated PPARα is associated with autophagy induction in chondrocytes is not determined. In this study, we investigated the effect of PPARα activation by its agonist, WY14643, on the protein expression level of Aggrecan and ADAMTS5, and the protein expression level of autophagy biomarkers, including LC3B and P62, using Western blotting analysis in isolated mouse chondrocytes pre-treated with lipopolysaccharides (LPS, mimicking OA chondrocytes) with or without the autophagy inhibitor chloroquine diphosphate salt. Furthermore, Akt and ERK phosphorylation was detected in LPS-treated chondrocytes in response to WY14643. In addition, the effect of intra-articularly injected WY14643 on articular cartilage in a mouse OA model established by the destabilization of the medial meniscus was assessed using the Osteoarthritis Research Society International (OARSI) histopathology assessment system, along with the detection of Aggrecan, ADAMTS5, LC3B and P62 protein levels using immunohistochemistry assay. The results indicated that PPARα activation by WY14643 promoted proteoglycan synthesis by autophagy enhancement in OA chondrocytes in vivo and in vitro concomitant with the elevation of Akt and ERK phosphorylation. Therefore, autophagy could contribute to the chondroprotection of PPARα activation by WY14643, with the implication that PPARα activation by WY14643 may be a potential approach for OA therapy.

Indexed as

AutophagyAnimalsAnticholesteremic AgentsCartilage, ArticularChondrocytesDisease Models, AnimalGene Expression RegulationLipopolysaccharidesMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLOsteoarthritisPPAR alphaProto-Oncogene Proteins c-aktPyrimidinesAnticholesteremic AgentsLipopolysaccharidespirinixic acidPPAR alphaProto-Oncogene Proteins c-aktPyrimidinesautophagymouse OA modelOA chondrocytePPARαWY14643

Identifiers

PMID30729704
PMCPMC6433667
OpenAlexW2915066966

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.