Evidence map›Paper›PMID 40346712›Full record

ArticleStem cell research & therapy2025

Human umbilical cord mesenchymal stem cell-derived exosomes repair IBD by activating the SIRT1-FXR pathway in macrophages.

Mengjiao Zhou, Bing Pei, Peipei Cai, Chengxue Yi, Francis Atim Akanyibah, Changkun Lyu, Fei Mao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

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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

16 citing papers in PubMed.

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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

7 authors.

Mengjiao ZhouDepartment of Laboratory Medicine, The Affiliated People's Hospital, Jiangsu University, No.8 Dianli Road, Zhenjiang, Jiangsu, 212002, P. R. China.
Bing PeiDepartment of Clinical Laboratory, The Affiliated Suqian First People's Hospital of Nanjing Medical University, Suqian, Jiangsu, 223800, P. R. China.
Peipei CaiDepartment of Laboratory Medicine, The Affiliated People's Hospital, Jiangsu University, No.8 Dianli Road, Zhenjiang, Jiangsu, 212002, P. R. China.
Chengxue YiSchool of Medical Technology, Zhenjiang College, Zhenjiang, Jiangsu, 212028, P. R. China.
Francis Atim AkanyibahDepartment of Laboratory Medicine, The Affiliated People's Hospital, Jiangsu University, No.8 Dianli Road, Zhenjiang, Jiangsu, 212002, P. R. China.
Changkun LyuSchool of Medical Technology, Shangqiu Medical College Shangqiu, Shangqiu, Henan, 476100, P. R. China.
Fei MaoDepartment of Laboratory Medicine, The Affiliated People's Hospital, Jiangsu University, No.8 Dianli Road, Zhenjiang, Jiangsu, 212002, P. R. China. maofei2003@ujs.edu.cn.ORCID http://orcid.org/0000-0001-5840-4436

Funding

Zhenjiang key research and development plan (social development) SH2023050
6 · The paper itself

Abstract

backgroundInflammatory bowel disease (IBD), a chronic immune disorder, has increasing global incidence and poor treatment outcome. Abnormal macrophage function is implicated in the pathophysiology of IBD. In this study, we investigated the mechanism by which human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Ex) inhibit inflammation in IBD mouse and macrophage inflammation models.

methodsWe established a dextran sodium sulfate (DSS)-induce BALB/c mice model of IBD and treated with hucMSC-Ex via tail vein to evaluate their repair effect on IBD mice. An in vitro macrophage inflammation model was established using lipopolysaccharide (LPS) and Nigericin (Nig) by stimulating mouse macrophage RAW264.7 and human myeloid leukemia mononuclear (THP-1) cells to assess the repair effect of hucMSC-Ex on macrophage inflammation. EX 527, an effective inhibitor of silent information regulator of transcription 1 (SIRT1), was employed in both the in vivo and in vitro models to explore the effect of hucMSC-Ex on the SIRT1-FXR (farnesoid X receptor) pathway in macrophages during the attenuation of inflammation.

resultsHucMSC-Ex effectively inhibited inflammation in both the in vivo and in vitro models by up-regulating the expressions of SIRT1 and FXR, which reduced the acetylation level of FXR and inhibited the activation of NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome. The addition of EX 527 further proved that hucMSC-Ex can reduce the acetylation of FXR by activating the SIRT1-FXR pathway, and the decrease of FXR acetylation was directly related to the inhibition of the activity of the NLRP3 inflammasome.

conclusionHucMSC-Ex alleviates IBD by reducing the acetylation level of FXR through activating the SIRT1-FXR pathway in macrophages and directly negatively regulating the activation of NLRP3 inflammasomes, thus inhibiting the occurrence of the inflammatory process.

Indexed as

ExosomesInflammatory Bowel DiseasesMacrophagesMesenchymal Stem CellsSirtuin 1AnimalsDextran SulfateDisease Models, AnimalHumansInflammasomesMaleMiceMice, Inbred BALB CNLR Family, Pyrin Domain-Containing 3 ProteinRAW 264.7 CellsSignal TransductionDextran SulfateInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinSIRT1 protein, humanSirtuin 1hucMSC-ExIBDMacrophageNLRP3 inflammasomeSIRT1-FXR pathway

Identifiers

PMID40346712
PMCPMC12065267

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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.