Evidence map›Paper›PMID 31852218›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2020

IL (Interleukin)-6 Contributes to Deep Vein Thrombosis and Is Negatively Regulated by miR-338-5p.

Yunhong Zhang, Zhen Zhang, Ran Wei, Xiuming Miao, Shangwen Sun, Gang Liang, Chu Chu, Lin Zhao, Xiaoxiao Zhu, Qiang Guo and 2 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
10.2field-weighted citation impact, top 1% 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

81 citing papers in PubMed, 129 citations in OpenAlex.

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  17. Pulmonary embolism in children with mycoplasma pneumonia: can it be predicted?European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025
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21 more citing papers are in PubMed but not listed here.

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 at 3 institutions in 1 country.

Yunhong ZhangFrom the School of Medicine and Life Sciences, University of Jinan-Shandong Academy of Medical Sciences, China (Y.Z., C.C.).
Zhen ZhangLaboratory for Molecular Immunology, Institute of Basic Medicine, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China (Y.Z., Z.Z., R.W., S.S., C.C., L.Z., X.Z., Q.G., X.L.).
Ran WeiLaboratory for Molecular Immunology, Institute of Basic Medicine, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China (Y.Z., Z.Z., R.W., S.S., C.C., L.Z., X.Z., Q.G., X.L.).
Xiuming MiaoDepartment of Peripheral Vascular Disease, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, China (X.M., G.L., B.W.).
Shangwen SunLaboratory for Molecular Immunology, Institute of Basic Medicine, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China (Y.Z., Z.Z., R.W., S.S., C.C., L.Z., X.Z., Q.G., X.L.).
Gang LiangDepartment of Peripheral Vascular Disease, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, China (X.M., G.L., B.W.).
Chu ChuFrom the School of Medicine and Life Sciences, University of Jinan-Shandong Academy of Medical Sciences, China (Y.Z., C.C.).
Lin ZhaoLaboratory for Molecular Immunology, Institute of Basic Medicine, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China (Y.Z., Z.Z., R.W., S.S., C.C., L.Z., X.Z., Q.G., X.L.).
Xiaoxiao ZhuLaboratory for Molecular Immunology, Institute of Basic Medicine, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China (Y.Z., Z.Z., R.W., S.S., C.C., L.Z., X.Z., Q.G., X.L.).
Qiang GuoLaboratory for Molecular Immunology, Institute of Basic Medicine, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China (Y.Z., Z.Z., R.W., S.S., C.C., L.Z., X.Z., Q.G., X.L.).
Bin WangDepartment of Peripheral Vascular Disease, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, China (X.M., G.L., B.W.).
Xia LiLaboratory for Molecular Immunology, Institute of Basic Medicine, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China (Y.Z., Z.Z., R.W., S.S., C.C., L.Z., X.Z., Q.G., X.L.).
Shandong First Medical University · CNAffiliated Hospital of Shandong University of Traditional Chinese Medicine · CNUniversity of Jinan · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveDeep venous thrombosis (DVT), one of the most common venous thromboembolic disorders, is closely linked with pulmonary embolism and post-thrombotic syndrome, both of which have a high mortality. However, the factors that trigger DVT formation are still largely unknown. Elevated expression of IL (interleukin)-6-an important inflammatory cytokine-has been linked with DVT formation. However, the molecular mechanisms leading to the elevated IL-6 in DVT remain unclear. Here, we proposed that epigenetic modification of IL-6 at the post-transcriptional level may be a crucial trigger for IL-6 upregulation in DVT. Approach and Results: To explore the association between microRNAs and IL-6 in DVT, we performed microRNA microarray analysis and experiments both in vitro and in vivo. Microarray and quantitative real-time polymerase chain reaction results showed that IL-6 expression was increased while miR-338-5p level was decreased substantially in peripheral blood mononuclear cells of patients with DVT, and there was significant negative correlation between miR-338-5p and IL-6. Experiments in vitro showed that overexpressed miR-338-5p reduced IL-6 expression, while miR-338-5p knockdown increased IL-6 expression. Moreover, our in vivo study found that mice with anti-IL-6 antibody or agomiR-338-5p delivery resulted in decreased IL-6 expression and alleviated DVT formation, whereas antagomiR-338-5p acted inversely. Most of miR-338-5p was found located in cytoplasm by fluorescence in situ hybridization. Dual-luciferase reporter assay identified direct binding between miR-338-5p and

conclusionsOur results suggest that decreased miR-338-5p promotes DVT formation by increasing IL-6 expression.

Indexed as

Gene Expression RegulationAngiographyAnimalsCells, CulturedEnzyme-Linked Immunosorbent AssayFemaleHumansInterleukin-6Lower ExtremityMaleMiceMice, Inbred C57BLMicroRNAsMiddle AgedRetrospective StudiesRNAInterleukin-6MicroRNAsMIRN338 microRNA, humanRNAcytoplasmfluorescenceinflammationinterleukin-6venous thrombosis

Identifiers

PMID31852218
PMCPMC6975520
OpenAlexW2996192796

What OpenQuestion holds

Textmetadata
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.