Evidence map›Paper›PMID 39350476›Full record

ArticleClinical and translational medicine2024

Adipose tissue-derived extracellular vesicles aggravate temporomandibular joint osteoarthritis associated with obesity.

Baochao Li, Yuqin Jin, Bingqing Zhang, Tong Lu, Jialing Li, Jingzi Zhang, Yiwen Zhou, Yanyi Wang, Caixia Zhang, Yue Zhao and 1 more

Abstract read
In one paragraph

Article in Clinical and translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

10 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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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

11 authors.

Baochao Li1Nanjing Stomatological Hospital & The State Key Laboratory of Pharmaceutical Biotechnology & Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, China.
Yuqin Jin1Nanjing Stomatological Hospital & The State Key Laboratory of Pharmaceutical Biotechnology & Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, China.
Bingqing Zhang1Nanjing Stomatological Hospital & The State Key Laboratory of Pharmaceutical Biotechnology & Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, China.
Tong Lu1Nanjing Stomatological Hospital & The State Key Laboratory of Pharmaceutical Biotechnology & Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, China.
Jialing Li1Nanjing Stomatological Hospital & The State Key Laboratory of Pharmaceutical Biotechnology & Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, China.
Jingzi Zhang1Nanjing Stomatological Hospital & The State Key Laboratory of Pharmaceutical Biotechnology & Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, China.
Yiwen Zhou1Nanjing Stomatological Hospital & The State Key Laboratory of Pharmaceutical Biotechnology & Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, China.
Yanyi Wang1Nanjing Stomatological Hospital & The State Key Laboratory of Pharmaceutical Biotechnology & Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, China.
Caixia Zhang1Nanjing Stomatological Hospital & The State Key Laboratory of Pharmaceutical Biotechnology & Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, China.
Yue Zhao1Nanjing Stomatological Hospital & The State Key Laboratory of Pharmaceutical Biotechnology & Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, China.
Huang Li1Nanjing Stomatological Hospital & The State Key Laboratory of Pharmaceutical Biotechnology & Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, China.ORCID 0000-0003-3910-3982

Funding

Fundamental Research Funds for the Central Universities 021414380536Key Project of the Health Commission of Jiangsu Province ZD2022025Key Project of the Nanjing Health Commission ZKX20048Nanjing Health Science and Technology Development Program YKK22178National Natural Science Foundation of China 32271182National Natural Science Foundation of China Special Project T2341015Natural Science Foundation for Excellent Young Scientists of Jiangsu Province BK20200061Natural Science Foundation of Jiangsu Province SBK2021021787
6 · The paper itself

Abstract

introductionTemporomandibular joint osteoarthritis (TMJ OA) is a major disease that affects maxillofacial health and is characterised by cartilage degeneration and subchondral bone remodelling. Obesity is associated with the exacerbation of pathological manifestations of TMJ OA. However, the underlying mechanism between adipose tissue and the TMJ axis remains limited.

objectivesTo evaluate the effects of obesity and the adipose tissue on the development of TMJ OA.

methodsThe obesity-related metabolic changes in TMJ OA patients were detected by physical signs and plasma metabolites. The effects of adipose tissue-derived EVs (Ad-EVs) on TMJ OA was investigated through histological and cytological experiments as well as gene editing technology. Alterations of Ad-EVs in obese state were identified by microRNA-seq analysis and the mechanism by which EVs affect TMJ OA was explored in vitro and in vivo.

resultsObesity and the related metabolic changes were important influencing factors for TMJ OA. Ad-EVs from obese mice induced marked chondrocyte apoptosis, cartilage matrix degradation and subchondral bone remodelling, which exacerbated the development of TMJ OA. Depletion of Ad-EVs secretion by knocking out the geranylgeranyl diphosphate synthase (Ggpps) gene in adipose tissue significantly inhibited the obesity-induced aggravation of TMJ OA. MiR-3074-5p played an important role in this process .

conclusionsOur work unveils an unknown link between obese adipose tissue and TMJ OA. Targeting the Ad-EVs and the miR-3074-5p may represent a promising therapeutic strategy for obesity-related TMJ OA. KEY POINTS: High-fat-diet-induced obesity aggravate the progression of TMJ OA in mice. Obese adipose tissue participates in cartilage damage through the altered miRNA in extracellular vesicles. Inhibition of miR-3074-5p/SMAD4 pathway in chondrocyte alleviated the effect of HFD-EVs on TMJ OA.

Indexed as

Adipose TissueExtracellular VesiclesObesityOsteoarthritisAnimalsDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLMicroRNAsTemporomandibular JointTemporomandibular Joint DisordersMicroRNAsadipose tissue‐derived extracellular vesiclesgeranylgeranyl diphosphate synthasemiR‐3074‐5ptemporomandibular joint osteoarthritis

Identifiers

PMID39350476
PMCPMC11442491

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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.