Evidence map›Paper›PMID 41831153›Full record

ArticleDigestive diseases and sciences2026

BECN1 Protects Against Intestinal Ischemia/Reperfusion Injury by Promoting NLRP3 Ubiquitination and Suppressing Inflammasome Activation.

Qiuhong Chen, Qian Hu, Zhen Liu, Qin Zhang, Jinping Nie, Qiong Wu, Sisi Liang, Yingjie Wang, Xuekang Zhang

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2026. 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

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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

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

9 authors.

Qiuhong ChenDepartment of Surgery and Anesthesia, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwai Zhengjie, Nanchang, 330006, Jiangxi, China.
Qian HuDepartment of Surgery and Anesthesia, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwai Zhengjie, Nanchang, 330006, Jiangxi, China.
Zhen LiuDepartment of Surgery and Anesthesia, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwai Zhengjie, Nanchang, 330006, Jiangxi, China.
Qin ZhangDepartment of Surgery and Anesthesia, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwai Zhengjie, Nanchang, 330006, Jiangxi, China.
Jinping NieDepartment of Surgery and Anesthesia, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwai Zhengjie, Nanchang, 330006, Jiangxi, China.
Qiong WuDepartment of Surgery and Anesthesia, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwai Zhengjie, Nanchang, 330006, Jiangxi, China.
Sisi LiangDepartment of Surgery and Anesthesia, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwai Zhengjie, Nanchang, 330006, Jiangxi, China.
Yingjie WangDepartment of Surgery and Anesthesia, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwai Zhengjie, Nanchang, 330006, Jiangxi, China.
Xuekang ZhangDepartment of Surgery and Anesthesia, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwai Zhengjie, Nanchang, 330006, Jiangxi, China. ndyfy00768@ncu.edu.cn.

Funding

National Natural Science Foundation of China 82260114Natural Science Foundation of Jiangxi Province 20232ACB206010
6 · The paper itself

Abstract

objectiveIntestinal ischemia/reperfusion (I/R) injury causes severe inflammation and disruption of the epithelial barrier, often leading to life-threatening complications. Although autophagy is known to provide tissue protection during I/R, the mechanisms linking autophagy to inflammasome regulation remain unclear. This study aimed to investigate the role of Beclin 1 (BECN1) in regulating NLRP3 inflammasome activation during intestinal I/R injury.

methodsIntestinal I/R models were used to examine changes in BECN1 expression in intestinal epithelial cells. Conditional knockout mice lacking Becn1 in intestinal epithelial cells were generated to evaluate its functional role in vivo. Autophagic flux, NLRP3 ubiquitination, inflammasome activation, and inflammatory cytokine production were assessed using molecular and biochemical approaches. In addition, the therapeutic potential of a cell-penetratingTAT-BECN1 peptide was evaluated in the I/R model.

resultsBECN1 expression was significantly upregulated in intestinal epithelial cells following I/R injury. Mechanistically, BECN1 promoted ubiquitin-dependent degradation of NLRP3, thereby limiting inflammasome activation. Conditional deletion of Becn1 in intestinal epithelial cells exacerbated intestinal injury and increased inflammatory cytokine production. Conversely, administration of the TAT-BECN1 peptide restored autophagic flux, enhanced NLRP3 ubiquitination, and attenuated epithelial damage and inflammation after I/R.

conclusionBECN1 protects against intestinal I/R injury by promoting NLRP3 ubiquitination and suppressing inflammasome activation through the autophagy pathway. These findings reveal a previously unrecognized mechanism linking autophagy to inflammasome regulation and suggest that targeting the BECN1-autophagy axis may represent a promising therapeutic strategy for intestinal I/R injury.

Indexed as

Beclin-1InflammasomesIntestinal MucosaNLR Family, Pyrin Domain-Containing 3 ProteinReperfusion InjuryAnimalsAutophagyEpithelial CellsMaleMiceMice, Inbred C57BLMice, KnockoutUbiquitinationBeclin-1Becn1 protein, mouseInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseAutophagyBeclin 1Intestinal ischemia/reperfusion injuryNLRP3 inflammasomeUbiquitination

Identifiers

PMID41831153

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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.