Evidence map›Paper›PMID 34457118›Full record

ArticleOxidative medicine and cellular longevity2021

Leptin Induced TLR4 Expression via the JAK2-STAT3 Pathway in Obesity-Related Osteoarthritis.

Mengqi Jiang, Jianyi He, Yingxu Sun, Xin Dong, Jiayu Yao, Hailun Gu, Li Liu

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

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  15. Relationship between Indel Variants within theAnimals : an open access journal from MDPI · 2024
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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

7 authors at 1 institution in 1 country.

Mengqi JiangDepartment of Nutrition and Food Hygiene, School of Public Health, China Medical University, 110122, China.ORCID https://orcid.org/0000-0003-3209-3443
Jianyi HeDepartment of Nutrition and Food Hygiene, School of Public Health, China Medical University, 110122, China.ORCID https://orcid.org/0000-0003-0343-6101
Yingxu SunDepartment of Nutrition and Food Hygiene, School of Public Health, China Medical University, 110122, China.ORCID https://orcid.org/0000-0001-8099-1964
Xin DongDepartment of Nutrition and Food Hygiene, School of Public Health, China Medical University, 110122, China.ORCID https://orcid.org/0000-0003-3487-4892
Jiayu YaoDepartment of Nutrition and Food Hygiene, School of Public Health, China Medical University, 110122, China.ORCID https://orcid.org/0000-0001-6242-9388
Hailun GuDepartment of Orthopedics, Shengjing Hospital, China Medical University, 110004, China.ORCID https://orcid.org/0000-0001-5697-9818
Li LiuDepartment of Nutrition and Food Hygiene, School of Public Health, China Medical University, 110122, China.ORCID https://orcid.org/0000-0001-5767-870X
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity is considered as a risk factor of osteoarthritis (OA), but the precise relationship is still poorly understood. Leptin, one of the most relevant factors secreted by adipose tissues, plays an important role in the pathogenesis of OA. Our aim was to investigate the regulation and molecular mechanism of the leptin signaling pathway in obesity-related OA. SD rats were fed with a high-fat diet (HFD) for 5, 15, and 27 weeks. The levels of leptin in serum increased from W5, while in the synovial fluid increased from W15. The histological evaluation showed that the pathological changes of OA occurred at 27 weeks rather than 5 or 15 weeks. We also found that leptin induced CD14/TLR4 activation by the JAK2-STAT3 signaling pathway to promote OA. Moreover, silencing SOCS3 enhanced leptin-induced JAK2-STAT3-CD14/TLR4 activation in rat primary chondrocytes. Our findings indicated that leptin may be one of the initiating factors of obesity-related OA. TLR4 is at least partially regulated by leptin through the JAK2-STAT3-CD14 pathway. Meanwhile, SOCS3 acting as a negative feedback inhibitor of leptin signaling presented a potential therapeutic prospect for obesity-related OA. Our study provided new evidence suggesting the key role of leptin in mediating obesity-related OA process and its underlying mechanisms.

Indexed as

Gene Expression RegulationAnimalsJanus Kinase 2LeptinMaleObesityOsteoarthritisRatsRats, Sprague-DawleySTAT3 Transcription FactorToll-Like Receptor 4Jak2 protein, ratJanus Kinase 2LeptinStat3 protein, ratSTAT3 Transcription FactorTlr4 protein, ratToll-Like Receptor 4

Identifiers

PMID34457118
PMCPMC8387187
OpenAlexW3194855463

What OpenQuestion holds

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Registered trials

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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.