Evidence map›Paper›PMID 41413572›Full record

ArticleArthritis research & therapy2025

RNF152-mediated, ubiquitin-dependent degradation of HSP27 activates the PI3K/AKT pathway, driving synovial inflammatory cascades in TMJOA.

Xinjian Zhang, Qingkun Jiang, Wei Deng, Hai Tang, Yang Liu, Zichen Xu, Ke Guo, Ning Liu, Haitao Wang, Tiehan Cui and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arthritis research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. In-depth analysis of retinal RNA transcriptome sequencing in a rat model of hypertensive retinopathy.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
    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

12 authors.

Xinjian Zhang *Jiangxi Provincial Key Laboratory of Department of Stomatology, The First Affiliated Hospital, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, China.
Qingkun Jiang *Jiangxi Provincial Key Laboratory of Department of Stomatology, The First Affiliated Hospital, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, China.
Wei Deng *Affiliated Stomatological Hospital of Gannan Medical University, Ganzhou, Jiangxi, 341000, China.
Hai Tang *Jiangxi Provincial Key Laboratory of Department of Stomatology, The First Affiliated Hospital, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, China.
Yang LiuJiangxi Provincial Key Laboratory of Department of Stomatology, The First Affiliated Hospital, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, China.
Zichen XuJiangxi Provincial Key Laboratory of Department of Stomatology, The First Affiliated Hospital, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, China.
Ke GuoJiangxi Provincial Key Laboratory of Department of Stomatology, The First Affiliated Hospital, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, China.
Ning LiuJiangxi Provincial Key Laboratory of Department of Stomatology, The First Affiliated Hospital, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, China.
Haitao WangJiangxi Provincial Key Laboratory of Department of Stomatology, The First Affiliated Hospital, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, China.
Tiehan CuiJiangxi Provincial Key Laboratory of Department of Stomatology, The First Affiliated Hospital, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, China.
Fang WangJiangxi Provincial Key Laboratory of Department of Stomatology, The First Affiliated Hospital, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, China.
Jiaxuan QiuJiangxi Provincial Key Laboratory of Department of Stomatology, The First Affiliated Hospital, Jiangxi Provincial Key Laboratory of Oral Diseases, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, China. xqiujiaxuan@163.com.

Funding

National Natural Science Foundation of China 82260194,82571102National Natural Science Foundation of China 82403716
6 · The paper itself

Abstract

backgroundE3 ubiquitin ligases are established regulators of osteoarthritis pathogenesis known to amplify inflammatory signals via substrate protein destabilization, but their role in temporomandibular joint osteoarthritis (TMJOA) remains elusive.

methodsThis study investigated the impact of E3 ligases on the activation of fibroblast-like synoviocytes (FLSs) in TMJOA and their mechanistic contributions to disease progression. High-throughput mRNA-sequencing identified dysregulated E3 ligases in interleukin-1β (IL-1β)–stimulated FLSs. Through integrated in vitro and in vivo analyses, we identified ring finger protein 152 (RNF152) as a key mediator of TMJOA pathogenesis. Comprehensive results from immunoprecipitation-mass spectrometry, co-immunoprecipitation, co-localization imaging, and protein docking demonstrated direct interaction between RNF152 and heat shock protein 27 (HSP27).

resultsIL-1β induced RNF152 upregulation while suppressing HSP27 expression in FLSs. Mechanistically, RNF152 ubiquitinated HSP27 at Lys114, making it a target for proteasomal degradation. Critically, RNF152-mediated HSP27 degradation activated the PI3K/AKT pathway, driving FLS proliferation and pro-inflammatory cytokine release, which accelerates TMJOA. Intra-articular delivery of adenovirus-associated virus-small interfering RNF152 attenuated synovial hyperplasia and chondrocyte damage in a rat model of TMJOA.

conclusionThis study elucidates the function of RNF152 as a novel E3 ligase and the dual regulatory role of HSP27 in inflammatory signaling. Importantly, our findings suggest that targeting the RNF152/HSP27/PI3K/AKT signaling axis may provide a novel therapeutic approach for TMJOA. Future research should focus on developing specific inhibitors to disrupt this pathway, thereby identifying promising therapeutic targets for targeted interventions in TMJOA.

Indexed as

HSP27 Heat-Shock ProteinsOsteoarthritisPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktUbiquitin-Protein LigasesAnimalsCells, CulturedHumansInflammationInterleukin-1betaMaleMolecular ChaperonesRatsRats, Sprague-DawleySignal TransductionSynovial MembraneHSP27 Heat-Shock ProteinsInterleukin-1betaMolecular ChaperonesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktUbiquitinUbiquitin-Protein LigasesE3 ubiquitin ligasesFibroblast-like synoviocytesHSP27PI3K/AKT signalling pathwayRNF152TMJOA

Identifiers

PMID41413572
PMCPMC12829216

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.