Evidence map›Paper›PMID 41540833›Full record

ArticleStem cells translational medicine2026

Human umbilical cord mesenchymal stem cells alleviate colon epithelial apoptosis in ulcerative colitis by activating inositol-requiring enzyme 1/X-box binding protein 1 signaling.

Taoran Zhao, Wenyi Hou, Mengwei Wang, Zhenyu Feng, Xiaoni Feng, Heng Wang, Hong Zhao, Xiujuan Li, Shulin Hou, Guoping Zheng and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cells translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

12 authors.

Taoran ZhaoDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan 030001, China.ORCID 0009-0009-9357-7928
Wenyi HouDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan 030001, China.
Mengwei WangDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan 030001, China.
Zhenyu FengShanxi Provincial Key Laboratory of Classical Prescription Strengthening Yang, Shanxi Hospital of Integrated Traditional and Western Medicine, Taiyuan 030001, China.
Xiaoni FengDepartment of Obstetrics and Gynecology, Shanxi Hospital of Integrated Traditional and Western Medicine, Taiyuan 030001, China.
Heng WangCentre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Sydney, NSW 2145, Australia.
Hong ZhaoDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan 030001, China.
Xiujuan LiDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan 030001, China.
Shulin HouDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan 030001, China.
Guoping ZhengCentre for Transplant and Renal Research, Westmead Institute for Medical Research, The University of Sydney, Sydney, NSW 2145, Australia.
Xiaozheng ZhangDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan 030001, China.
Jun XieDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan 030001, China.

Funding

Natural Science Foundation of Shanxi Province 20210302123315Natural Science Foundation of Shanxi Province 202303021221128
6 · The paper itself

Abstract

backgroundUlcerative colitis (UC), a chronic inflammatory gastrointestinal disease, is characterized by disrupted intestinal barrier integrity and unresolved endoplasmic reticulum (ER) stress, which drives epithelial apoptosis and disease progression. While mesenchymal stem cells (MSCs), particularly human umbilical cord-derived MSCs (hUC-MSCs), have shown therapeutic potential in UC, their mechanisms in modulating ER stress remain unclear. This study aimed to investigate the role of hUC-MSCs in alleviating ER stress-induced epithelial damage and elucidate the underlying molecular pathways in a murine colitis model and in vitro systems.

resultsIntraperitoneal administration of hUC-MSCs significantly attenuated dextran sulfate sodium (DSS)-induced colitis in mice. Histological analysis revealed restored crypt architecture and reduced epithelial apoptosis. Transcriptomic profiling demonstrated that hUC-MSCs reduced differentially expressed genes in inflammatory bowel disease-related and ER stress response pathways in colon tissues. Mechanistically, hUC-MSCs activated the IRE1/XBP1 axis, increasing Xbp1 splicing and suppressing pro-apoptotic Bcl2l11 expression. In vitro, hUC-MSC-conditioned medium protected colon epithelial cells from TNF-α-induced apoptosis via IRE1/XBP1 activation, an effect abolished by the IRE1 inhibitor 4μ8C.

conclusionsOur findings demonstrate that hUC-MSCs alleviate UC by mitigating ER stress through IRE1-mediated Xbp1 splicing, thereby reducing epithelial apoptosis and promoting mucosal repair. This study provides a mechanistic foundation for MSC-based therapies targeting ER stress in inflammatory bowel diseases.

Indexed as

ApoptosisColitis, UlcerativeColonEndoribonucleasesMesenchymal Stem CellsMesenchymal Stem Cell TransplantationProtein Serine-Threonine KinasesUmbilical CordX-Box Binding Protein 1AnimalsDextran SulfateDisease Models, AnimalEndoplasmic Reticulum StressEpithelial CellsHumansIntestinal MucosaDextran SulfateEndoribonucleasesERN1 protein, humanProtein Serine-Threonine KinasesX-Box Binding Protein 1XBP1 protein, humanendoplasmic reticulum stressintestinal epithelial apoptosisIRE1/XBP1 signalingmesenchymal stem cellsmucosal repairulcerative colitis

Identifiers

PMID41540833
PMCPMC12808544

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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.