Evidence map›Paper›PMID 38844123›Full record

ArticleJournal of advanced research2025

GYY4137-induced p65 sulfhydration protects synovial macrophages against pyroptosis by improving mitochondrial function in osteoarthritis development.

Jun Ma, Peng Yang, Zhibin Zhou, Tengfei Song, Liang Jia, Xiaofei Ye, Wei Yan, Jiuyi Sun, Tianwen Ye, Lei Zhu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed.

  1. Article
  2. Review
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  8. Article
  9. Calcium sulfide nanoparticles as sustained HFrontiers in immunology · 2026
    Article
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  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  17. Review
  18. Review
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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

10 authors.

Jun MaDepartment of Orthepaedics, Naval Medical Center of PLA, Naval Medical University, Shanghai, China; Department of Health Statistics, Naval Medical University, Shanghai, China; Department of Orthopaedic Trauma Surgery, Shanghai Changzheng Hospital, Naval Medical University, Shanghai, China.
Peng YangDepartment of Orthepaedics, Naval Medical Center of PLA, Naval Medical University, Shanghai, China; Department of Orthopaedic Trauma Surgery, Shanghai Changzheng Hospital, Naval Medical University, Shanghai, China.
Zhibin ZhouDepartment of Orthopaedic Trauma Surgery, Shanghai Changzheng Hospital, Naval Medical University, Shanghai, China; Department of Orthopaedics, General Hospital of Northern Theater Command, Shenyang, Liaoning, China.
Tengfei SongDepartment of Orthopaedic Trauma Surgery, Shanghai Changzheng Hospital, Naval Medical University, Shanghai, China.
Liang JiaCollege of Fisheries and Life Science, Shanghai Ocean University, Shanghai, China.
Xiaofei YeDepartment of Health Statistics, Naval Medical University, Shanghai, China.
Wei YanDepartment of Orthepaedics, Naval Medical Center of PLA, Naval Medical University, Shanghai, China.
Jiuyi SunDepartment of Orthepaedics, Naval Medical Center of PLA, Naval Medical University, Shanghai, China. Electronic address: sunjiuyi@smmu.edu.cn.
Tianwen YeDepartment of Orthopaedic Trauma Surgery, Shanghai Changzheng Hospital, Naval Medical University, Shanghai, China. Electronic address: Yetianwenvip@126.com.
Lei ZhuDepartment of Orthopaedic Trauma Surgery, Shanghai Changzheng Hospital, Naval Medical University, Shanghai, China. Electronic address: hailangzhulei@smmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionOsteoarthritis (OA) is the most common arthritis that is characterized by the progressive synovial inflammation and loss of articular cartilage. Although GYY4137 is a novel and slow-releasing hydrogen sulfide (H

objectivesIn this study, we validated the protective role of GYY4137 against OA pathological courses and elucidated its underlying regulatory mechanisms.

methodsCell transfection, immunofluorescence staining, EdU assay, transmission electron microscopy, mitochondrial membrane potential measurement, electrophoretic mobility shift assay, sulfhydration assay, qPCR and western blot assays were performed in the primary mouse chondrocytes or the mouse macrophage cell line raw 264.7 for in vitro study. DMM-induced OA mice model and Macrophage-specific p65 knockout (p65

resultsWe found that GYY4137 can alleviate OA progress by suppressing synovium pyroptosis in vivo. Moreover, our in vitro data revealed that GYY4137 attenuates inflammation-induced NLRP3 and caspase-1 activation and results in a decrease of IL-1β production in macrophages. Mechanistically, GYY4137 increased persulfidation of NF-kB p65 in response to inflammatory stimuli that results in a decrease of cellular reactive oxygen species (ROS) accumulation and ameliorates mitochondrial dysfunctions. Using site-directed mutagenesis, we showed that H

conclusionThese findings suggest a mechanism by which GYY4137 through redox modification of p65 participates in inhibiting NLRP3 activation by OA to regulate inflammatory responses. Thus, we propose that GYY4137 represents a promising novel therapeutic strategy for the treatment of OA.

Indexed as

MacrophagesMitochondriaMorpholinesOrganothiophosphorus CompoundsOsteoarthritisPyroptosisTranscription Factor RelAAnimalsChondrocytesDisease Models, AnimalMaleMiceMice, Inbred C57BLMice, KnockoutNLR Family, Pyrin Domain-Containing 3 ProteinRAW 264.7 CellsGYY 4137MorpholinesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseOrganothiophosphorus CompoundsRela protein, mouseTranscription Factor RelA

Identifiers

PMID38844123
PMCPMC12126715

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.