Evidence map›Paper›PMID 41954769›Full record

ArticlePancreas2026

The IL-33/ST2 Signaling Axis Alleviates Splenic Injury in Severe Acute Pancreatitis by Inhibiting T-Cell Ferroptosis.

Lijian Cui, Ning Xu, Jianhong Chen, Chuxuan Bin, Yue Feng, Baona Guo, Enjie Zhang, Yingyi Luan, Chenghong Yin

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pancreas, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Lijian CuiDepartment of Central Laboratory, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing Maternal and Child Health Care Hospital, Beijing, China.
Ning XuDepartment of Central Laboratory, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing Maternal and Child Health Care Hospital, Beijing, China.
Jianhong ChenDepartment of Gastroenterology, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Chuxuan BinDepartment of Gastroenterology, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Yue FengDepartment of Gastroenterology, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Baona GuoDepartment of Gastroenterology, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Enjie ZhangDepartment of Central Laboratory, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing Maternal and Child Health Care Hospital, Beijing, China.
Yingyi LuanDepartment of Central Laboratory, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing Maternal and Child Health Care Hospital, Beijing, China.
Chenghong YinDepartment of Central Laboratory, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing Maternal and Child Health Care Hospital, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThis study aimed to investigate whether the IL-33/ST2 signaling axis alleviates SAP-induced splenic injury by regulating ferroptosis in T lymphocytes.

methodsA murine SAP model was established through intraperitoneal injection of cerulein and lipopolysaccharide (LPS). Recombinant IL-33 was administered intraperitoneally. Histopathologic changes, inflammatory cytokines, ferroptosis-related indicators (MDA, Fe 2+ , GSH, GPX4, ACSL4, FTH1), mitochondrial function [mtDNA, ATP, mitochondrial ROS (mito-SOX), and membrane potential], and ultrastructural alterations were assessed. In vitro, Concanavalin A-stimulated splenic T cells were treated with IL-33, the ferroptosis inhibitor Ferrostatin-1 (Fer-1), or the ST2 antagonist soluble ST2 (sST2) to validate the pathway.

resultsIL-33 treatment significantly alleviated pancreatic and splenic histopathologic damage, reduced systemic inflammation, and inhibited ferroptosis in the spleen, as evidenced by attenuated lipid peroxidation, attenuated glutathione depletion, and normalized expression of key ferroptosis regulators (GPX4, ACSL4, FTH1). Concurrently, IL-33 improved mitochondrial function and attenuated oxidative stress. In vitro, IL-33 directly inhibited ConA-induced T-cell ferroptosis, an effect mimicked by Fer-1. Crucially, all protective effects of IL-33 were abolished by sST2, confirming that its action is specifically dependent on the ST2 receptor.

conclusionsThe IL-33/ST2 axis exerts a protective effect in SAP by inhibiting T-cell ferroptosis, improving mitochondrial function, and maintaining redox homeostasis, highlighting its potential as a therapeutic target.

Indexed as

FerroptosisInterleukin-1 Receptor-Like 1 ProteinInterleukin-33PancreatitisSpleenT-LymphocytesAcute DiseaseAnimalsCeruletideDisease Models, AnimalMaleMiceMice, Inbred C57BLMitochondriaSignal TransductionCeruletideIl1rl1 protein, mouseIl33 protein, mouseInterleukin-1 Receptor-Like 1 ProteinInterleukin-33ferroptosisIL-33mitochondrial dysfunctionsevere acute pancreatitisST2T lymphocytes

Identifiers

PMID41954769
PMCPMC13348841

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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.