Evidence map›Paper›PMID 40416374›Full record

ArticleFrontiers in nutrition2025

Iron modulates barrier integrity and stem cell function of small intestine during experimental colitis.

Shubin Wang, Xiangjie Yang, Xiangjun Liu, Qin Wen, Lu Xu, Mei Feng, Jinyi Lang, Dengqun Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in nutrition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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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3 · Its place in the literature

Who cites it

3 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

8 authors.

Shubin Wang *Radiation Oncology Key Laboratory of Sichuan Province, Sichuan Cancer Hospital and Institute, Sichuan Provincial Engineering Research Center for Tumor Organoids and Clinical Transformation, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Xiangjie Yang *Radiation Oncology Key Laboratory of Sichuan Province, Sichuan Cancer Hospital and Institute, Sichuan Provincial Engineering Research Center for Tumor Organoids and Clinical Transformation, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Xiangjun Liu *Radiation Oncology Key Laboratory of Sichuan Province, Sichuan Cancer Hospital and Institute, Sichuan Provincial Engineering Research Center for Tumor Organoids and Clinical Transformation, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Qin WenRadiation Oncology Key Laboratory of Sichuan Province, Sichuan Cancer Hospital and Institute, Sichuan Provincial Engineering Research Center for Tumor Organoids and Clinical Transformation, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Lu XuRadiation Oncology Key Laboratory of Sichuan Province, Sichuan Cancer Hospital and Institute, Sichuan Provincial Engineering Research Center for Tumor Organoids and Clinical Transformation, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Mei FengRadiation Oncology Key Laboratory of Sichuan Province, Sichuan Cancer Hospital and Institute, Sichuan Provincial Engineering Research Center for Tumor Organoids and Clinical Transformation, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Jinyi LangRadiation Oncology Key Laboratory of Sichuan Province, Sichuan Cancer Hospital and Institute, Sichuan Provincial Engineering Research Center for Tumor Organoids and Clinical Transformation, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Dengqun LiuRadiation Oncology Key Laboratory of Sichuan Province, Sichuan Cancer Hospital and Institute, Sichuan Provincial Engineering Research Center for Tumor Organoids and Clinical Transformation, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Ulcerative colitis (UC) brings inconvenience to many patients with inflammatory bowel disease (IBD). Although colonic pathology is widely investigated, little attention has been paid to the disorders in small intestine of UC. In this study, we investigated the impairments of UC to small intestine and further explored how iron metabolism regulated epithelial integrity and the activity of intestinal stem cells (ISCs). Methods: Mice were treated by 2.5% dextran sulfate sodium (DSS) for 7 days to established acute experimental colitis. Small intestinal tissues were collected at different time points in the process of DSS-induced colitis. Histological analysis was used to evaluate the changes of small intestine, including H&E, Alcian blue and PAS staining, immunostaining, and qRT-PCR. Iron content was modulated by the supplementation of ferric citrate or depletion by deferoxamine (DFO). The influence of iron on the barrier integrity and stem cell function was further determined by histology, IEC-6 cell, and enteroid culture. ROS content was demonstrated by DHE staining. The proliferation of intestinal stem cells (ISCs) was shown by BrdU and Olfm4 staining, and Lgr5-tdTomato mice were used for lineage tracing study. Results: It was shown that during DSS-induced colitis, small intestine underwent a serious injury process, including dysregulated integrity and decreased proliferation of ISCs. Iron overload significantly exacerbated intestinal injury in tissues, epithelial cell line, and intestinal organoids. However, iron chelation by deferoxamine (DFO) would greatly suppress small intestinal injury. Mechanistically, iron overload exacerbated the generation of ROS and enhanced the infiltration of immune cells. In addition, STAT3 and ERK pathways in intestinal epithelium were impaired during experimental colitis, and iron content significantly interrupted the expression of p-STAT3 and p-ERK1/2 within small intestine. Conclusion: In summary, this study proved that small intestine was also impaired in experimental colitis, and iron content could affect DSS-induced small intestinal damage and regeneration, indicating the strategy of iron supplementation in clinical practice needs to be more cautious and consider more factors.

Indexed as

acute experimental colitisDFOintestinal stem cellironorganoid

Identifiers

PMID40416374
PMCPMC12100934

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