Evidence map›Paper›PMID 42014617›Full record

ArticleInflammation2026

Dendritic Cells Derived MMP9 Fuels Sepsis-Induced Cardiac Dysfunction Through JNK/AP1 Driven Pro-Inflammatory Cytokine and Nitric Oxide Storm.

Jiewen Deng, Yulan Qu, Yanyan Jiang, Yao Xie, Xiaotian Ma, Jian Shen, Zhenhong Guo, Meixiang Xiang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Inflammation, 2026. 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. Review
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

8 authors.

Jiewen Deng *Department of Cardiology, State Key Laboratory of Transvascular Implantation Devices, The Second Affiliated Hospital, Zhejiang University School of Medicine, 88 Jiefang Road, Hangzhou, Zhejiang, 310009, China.
Yulan Qu *Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Yanyan Jiang *NHC Key Laboratory of Parasite and Vector Biology, National Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention (Chinese Center for Tropical Diseases Research), Shanghai, 200025, China.
Yao XieDepartment of Cardiology, State Key Laboratory of Transvascular Implantation Devices, The Second Affiliated Hospital, Zhejiang University School of Medicine, 88 Jiefang Road, Hangzhou, Zhejiang, 310009, China.
Xiaotian MaNational Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, 200433, China.
Jian ShenDepartment of Cardiology, State Key Laboratory of Transvascular Implantation Devices, The Second Affiliated Hospital, Zhejiang University School of Medicine, 88 Jiefang Road, Hangzhou, Zhejiang, 310009, China.
Zhenhong GuoNational Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, 200433, China. guozh@immunol.org.
Meixiang XiangDepartment of Cardiology, State Key Laboratory of Transvascular Implantation Devices, The Second Affiliated Hospital, Zhejiang University School of Medicine, 88 Jiefang Road, Hangzhou, Zhejiang, 310009, China. xiangmx@zju.edu.cn.

Funding

National Key R&D Program of China New strategies of immune tolerance induction in human stem cells allotransplantation No. 2017YFA0104402Shanghai Sailing Program 21YF1459000the National Nature Science Foundation of China 81870203
6 · The paper itself

Abstract

Metalloproteinase9 is an important inflammatory mediator, but its contribution to sepsis-induced myocardial dysfunction (SIMD) remains unclear. In this study, we found that MMP9 deletion in mice evoked resistance to LPS-triggered septic cardiac dysfunction and lethality, accompanied by heavily reduced serum level of inflammatory factors and the myocardial damage markers. Similar results were acquired when an MMP9 inhibitor was used to treat LPS-induced sepsis, indicating that MMP9 promoted the progression of SIMD. It is well-known that DCs can induce inflammatory response to promote septic tissue damage. Notably, MMP9-/- BMDCs were significantly more effective in reducing sepsis-induced myocardial dysfunction compared to WT BMDCs. Mechanistically, MMP9 deficiency in BMDCs mainly curtailed the release of IL-6, IL-1β, IL-17 A, and nitric oxide via the JNK/AP1 pathway, thus safeguarding cardiomyocytes from death. Collectively, this study contributed new insights into the role of MMP9 in DCs within the context of SIMD.

Indexed as

CytokinesDendritic CellsInflammation MediatorsMatrix Metalloproteinase 9Nitric OxideSepsisTranscription Factor AP-1AnimalsMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacCytokinesInflammation MediatorsMatrix Metalloproteinase 9Mmp9 protein, mouseNitric OxideTranscription Factor AP-1BMDCsInflammatory cytokineMatrix metalloproteinases 9 (MMP9)SIMD

Identifiers

PMID42014617
PMCPMC13233659

What OpenQuestion 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 OpenQuestion graph.