Evidence map›Paper›PMID 40678707›Full record

ArticleWorld journal of gastroenterology2025

Paneth cells inhibit intestinal stem cell proliferation through the bone morphogenic protein 7 pathway under rotavirus-mediated intestinal injury.

Xiang-Yi Bu, Hao-Yuan Tan, An-Min Wang, Ming-Tong Wei, Sophie Pan, Juan-Zi Gao, Yong-Hai Li, Gui-Xiang Qian, Zi-Han Chen, Chao Ye and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in World journal of gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

11 authors.

Xiang-Yi BuDepartment of Hepatic Surgery, Anhui Provincial Hospital, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Science and Medicine, University of Science and Technology of China, Hefei 230001, Anhui Province, China.
Hao-Yuan TanDepartment of Digestive Disease, Anhui Provincial Hospital, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Science and Medicine, University of Science and Technology of China, Hefei 230001, Anhui Province, China.
An-Min WangDepartment of Digestive Disease, Anhui Provincial Hospital, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Science and Medicine, University of Science and Technology of China, Hefei 230001, Anhui Province, China.
Ming-Tong WeiDepartment of Hepatic Surgery, Anhui Provincial Hospital Affiliated to Anhui Medical University, Hefei 230001, Anhui Province, China.
Sophie PanDepartment of Life Sciences, University of California, Los Alamitos, CA 90025, United States.
Juan-Zi GaoDepartment of Hepatic Surgery, Anhui Provincial Hospital, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Science and Medicine, University of Science and Technology of China, Hefei 230001, Anhui Province, China.
Yong-Hai LiHefei First People's Hospital, The Third Affiliated Hospital of Anhui Medical University, Hefei 230001, Anhui Province, China.
Gui-Xiang QianHefei First People's Hospital, The Third Affiliated Hospital of Anhui Medical University, Hefei 230001, Anhui Province, China.
Zi-Han ChenDepartment of Hepatic Surgery, Anhui Provincial Hospital, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Science and Medicine, University of Science and Technology of China, Hefei 230001, Anhui Province, China.
Chao YeDepartment of Digestive Disease, Anhui Provincial Hospital, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Science and Medicine, University of Science and Technology of China, Hefei 230001, Anhui Province, China.
Wei-Dong JiaDepartment of Hepatic Surgery, Anhui Provincial Hospital, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Science and Medicine, University of Science and Technology of China, Hefei 230001, Anhui Province, China. jwd1968@ustc.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRotavirus (RV), a primary cause of diarrhea-related mortality in 2021, has been shown to damage intestinal epithelial cells while upregulating intestinal stem cells (ISCs) activities. ISCs within the crypt niche drive the continuous self-renewal of intestinal epithelium, preserving its barrier functions. Paneth cells secrete antimicrobial peptide and signaling molecules within the intestine crypt, thereby playing a crucial role in intestinal immune defense and providing ISCs functional support. However, the regulatory function of Paneth cells under pathological conditions, such as RV infection, remains unclear.

aimTo determine the impact of RV infection on Paneth cells and how Paneth cells regulate ISCs during intestinal injury repair.

methodsWe constructed a reference genome for the RV enteric cytopathogenic human orphan virus strain and reanalyzed published single-cell RNA sequencing data to investigate Paneth cell responses to RV-induced intestinal injury. We derived Paneth-ISC communication networks using CellChat, tracked ISC differentiation with pseudotime analysis, and validated our findings in leucine-rich repeat-containing G protein-coupled receptor 5-enhanced green fluorescent protein-internal ribosomal entry site-Cre recombinase estrogen receptor variant 2 mice and organoids

resultsWe found that RV directly infects Paneth cells, leading to a reduction in mature Paneth cells and an increase in kallikrein 1-high immature Paneth cells. Paneth-ISC communication was significantly enhanced. In particular, the bone morphogenic protein 7 (BMP7)-activin A receptor type 2B/BMP receptor type 1A-Smad pathway was upregulated post-infection, suggesting that Paneth cells suppress excessive ISC proliferation. Functional validation confirmed activation of this pathway.

conclusionPaneth cells regulate ISC proliferation during RV infection by activating BMP7 signaling, limiting excessive stem cell expansion and preserving crypt homeostasis for effective epithelial repair.

Indexed as

Bone Morphogenetic Protein 7Intestinal MucosaPaneth CellsRotavirusRotavirus InfectionsStem CellsAnimalsCell DifferentiationCell ProliferationDisease Models, AnimalHumansMiceMice, Inbred C57BLOrganoidsSignal TransductionBone Morphogenetic Protein 7Bone morphogenetic protein 7Intestinal injuryIntestinal stem cellsPaneth cellsRotavirus infection

Identifiers

PMID40678707
PMCPMC12264854

What Socratic holds

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LicenceCC BY-NC
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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 Socratic graph.