Evidence map›Paper›PMID 37094666›Full record

ArticleJournal of advanced research2024

The miR-7/EGFR axis controls the epithelial cell immunomodulation and regeneration and orchestrates the pathology in inflammatory bowel disease.

Juanjuan Zhao, Mengmeng Guo, Yaping Yan, Ya Wang, Xu Zhao, Jing Yang, Jing Chen, Chao Chen, Lin Tang, Wenhuan Zeng and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of advanced research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

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  6. [Pinostrobin targets the PI3K/AKT/CCLNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
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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

14 authors at 1 institution in 1 country.

Juanjuan ZhaoSchool of Medicine, Guizhou University, Guiyang 550025, Guizhou, China; Department of Immunology, Zunyi Medical University, Guizhou 563000, China; Key Laboratory of Gene Detection and Treatment of Guizhou Province, Guizhou, Zunyi 563000, China.
Mengmeng GuoDepartment of Immunology, Zunyi Medical University, Guizhou 563000, China; Key Laboratory of Gene Detection and Treatment of Guizhou Province, Guizhou, Zunyi 563000, China.
Yaping YanDepartment of Immunology, Zunyi Medical University, Guizhou 563000, China; Key Laboratory of Gene Detection and Treatment of Guizhou Province, Guizhou, Zunyi 563000, China.
Ya WangDepartment of Immunology, Zunyi Medical University, Guizhou 563000, China; Key Laboratory of Gene Detection and Treatment of Guizhou Province, Guizhou, Zunyi 563000, China.
Xu ZhaoDepartment of Immunology, Zunyi Medical University, Guizhou 563000, China; Key Laboratory of Gene Detection and Treatment of Guizhou Province, Guizhou, Zunyi 563000, China.
Jing YangDepartment of Immunology, Zunyi Medical University, Guizhou 563000, China; Key Laboratory of Gene Detection and Treatment of Guizhou Province, Guizhou, Zunyi 563000, China.
Jing ChenDepartment of Immunology, Zunyi Medical University, Guizhou 563000, China; Key Laboratory of Gene Detection and Treatment of Guizhou Province, Guizhou, Zunyi 563000, China.
Chao ChenDepartment of Immunology, Zunyi Medical University, Guizhou 563000, China; Key Laboratory of Gene Detection and Treatment of Guizhou Province, Guizhou, Zunyi 563000, China.
Lin TangDepartment of Immunology, Zunyi Medical University, Guizhou 563000, China; Key Laboratory of Gene Detection and Treatment of Guizhou Province, Guizhou, Zunyi 563000, China.
Wenhuan ZengKey Laboratory of Gene Detection and Treatment of Guizhou Province, Guizhou, Zunyi 563000, China.
Yiting LiuKey Laboratory of Gene Detection and Treatment of Guizhou Province, Guizhou, Zunyi 563000, China.
Ming QinDepartment of Immunology, Zunyi Medical University, Guizhou 563000, China; Key Laboratory of Gene Detection and Treatment of Guizhou Province, Guizhou, Zunyi 563000, China.
Ya ZhouDepartment of Medical Physics, Zunyi Medical University, Guizhou 563000, China; Key Laboratory of Gene Detection and Treatment of Guizhou Province, Guizhou, Zunyi 563000, China.
Lin XuSchool of Medicine, Guizhou University, Guiyang 550025, Guizhou, China; Department of Immunology, Zunyi Medical University, Guizhou 563000, China; Key Laboratory of Gene Detection and Treatment of Guizhou Province, Guizhou, Zunyi 563000, China; Collaborative Innovation Center of Tissue Damage Repair and Regeneration Medicine of Zunyi Medical University, Zunyi, Guizhou 563000, China. Electronic address: xulinzhouya@163.com.
Zunyi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe epithelial immunomodulation and regeneration are intrinsic critical events against inflammatory bowel disease (IBD). MiR-7 is well documented as a promising regulator in the development of various diseases including inflammatory diseases.

objectivesThis study aimed to assess the effect of miR-7 in intestinal epithelial cells (IECs) in IBD.

methodsMiR-7

resultsWe found miR-7 deficiency improved the pathological lesions of DSS-induced murine enteritis model, accompanied by elevated proliferation and enhanced transduction of NF-κB/AKT/ERK signals in colonic IECs, as well as decreased local infiltration of inflammatory cells. MiR-7 was dominantly upregulated in colonic IECs in colitis. Moreover, the transcription of pre-miR-7a-1, orchestrated by transcription factor C/EBPα, was a main resource of mature miR-7 in IECs. As for the mechanism, EGFR, a miR-7 target gene, was downregulated in colonic IECs in colitis model and Crohn's disease patients. Furthermore, miR-7 also controlled the proliferation and inflammatory-cytokine secretion of IECs in response to inflammatory-signals through EGFR/NF-κB/AKT/ERK pathway. Finally, IEC-specific miR-7 silencing promoted the proliferation and transduction of NF-κB pathway in IECs and alleviated the pathological damage of colitis.

conclusionOur results present the unknown role of miR-7/EGFR axis in IEC immunomodulation and regeneration in IBD and might provide clues for the application of miRNA-based therapeutic strategies in colonic diseases.

Indexed as

ColitisEnteritisInflammatory Bowel DiseasesMicroRNAsAnimalsEpithelial CellsErbB ReceptorsHumansMiceNF-kappa BProto-Oncogene Proteins c-aktRegenerationEGFR protein, humanErbB ReceptorsMicroRNAsMIRN7-1 microRNA, humanNF-kappa BProto-Oncogene Proteins c-aktEGFRImmune cellsInflammatory bowel diseaseIntestinal epithelial cellsMiR-7

Identifiers

PMID37094666
PMCPMC10918346
OpenAlexW4366748211

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.