Evidence map›Paper›PMID 41923629›Full record

ArticleCell reports. Medicine2026

Gut-microbiota-derived 3-indoleacrylic acid alleviates neonatal necrotizing enterocolitis by inhibiting epithelial necroptosis.

Xiaoliang Dong, Mengwen Wang, Bingxin Wang, Hongli Li, Zeyun Cao, Binbin Li, Xun Zou, Xuan Kong, Huanxin Yang, Yufeng Zhou and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports. Medicine, 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

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

13 authors.

Xiaoliang DongDepartment of Neonatology, Affiliated Children's Hospital of Jiangnan University (Wuxi Children's Hospital), Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China; MOE Medical Basic Research Innovation Center for Gut Microbiota and Chronic Diseases, Jiangnan University, Wuxi, Jiangsu 214122, China.
Mengwen WangDepartment of Neonatology, Affiliated Children's Hospital of Jiangnan University (Wuxi Children's Hospital), Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China; MOE Medical Basic Research Innovation Center for Gut Microbiota and Chronic Diseases, Jiangnan University, Wuxi, Jiangsu 214122, China.
Bingxin WangDepartment of Neonatology, Affiliated Children's Hospital of Jiangnan University (Wuxi Children's Hospital), Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China; MOE Medical Basic Research Innovation Center for Gut Microbiota and Chronic Diseases, Jiangnan University, Wuxi, Jiangsu 214122, China.
Hongli LiDepartment of Neonatology, Affiliated Children's Hospital of Jiangnan University (Wuxi Children's Hospital), Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China.
Zeyun CaoDepartment of Neonatology, Affiliated Children's Hospital of Jiangnan University (Wuxi Children's Hospital), Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China.
Binbin LiSchool of Life Sciences and Health Engineering, Jiangnan University, Wuxi 214122, China; School of Food Science and Technology, Jiangnan University, Wuxi 214122, China.
Xun ZouDepartment of Neonatology, Affiliated Children's Hospital of Jiangnan University (Wuxi Children's Hospital), Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China.
Xuan KongDepartment of Neonatology, Affiliated Children's Hospital of Jiangnan University (Wuxi Children's Hospital), Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China.
Huanxin YangDepartment of Neonatology, Affiliated Children's Hospital of Jiangnan University (Wuxi Children's Hospital), Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China.
Yufeng ZhouInstitute of Pediatrics, Children's Hospital of Fudan University, National Children's Medical Center, and the Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Le ZhangDepartment of Neonatology, Affiliated Children's Hospital of Jiangnan University (Wuxi Children's Hospital), Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China; Clinical Research Center, Affiliated Children's Hospital of Jiangnan University, Wuxi Children's Hospital, Jiangsu Provincial Industrial Technology Engineering Center for Pediatric Metabolic Disease Prevention and Control, Wuxi Key Laboratory of Genetic and Metabolic Diseases in Children, Wuxi 214023, Jiangsu, China. Electronic address: zhangle@jiangnan.edu.cn.
Li-Long PanDepartment of Neonatology, Affiliated Children's Hospital of Jiangnan University (Wuxi Children's Hospital), Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China; MOE Medical Basic Research Innovation Center for Gut Microbiota and Chronic Diseases, Jiangnan University, Wuxi, Jiangsu 214122, China. Electronic address: llpan@jiangnan.edu.cn.
Jia SunSchool of Life Sciences and Health Engineering, Jiangnan University, Wuxi 214122, China; School of Food Science and Technology, Jiangnan University, Wuxi 214122, China. Electronic address: jiasun@jiangnan.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neonatal necrotizing enterocolitis (NEC) is a severe inflammatory disease primarily affecting premature infants, characterized by high mortality and morbidity, with limited therapeutic options available. While emerging evidence links microbiota to NEC pathogenesis, the role of commensal metabolites in NEC and safe metabolite-based therapies remain unexplored. Metabolomic profiling reveals a significant reduction in 3-indoleacrylic acid (IA), a tryptophan-derived metabolite, in NEC infants and animal models. IA supplementation alleviates intestinal inflammation and tissue damage. Single-cell RNA sequencing analysis reveals the activation of STAT1 signaling as a necroptosis driver in intestinal epithelial cells, which is suppressed by IA. Protection is abolished by aryl hydrocarbon receptor (AhR) inhibitor CH-223191 or in intestinal epithelium-specific AhR knockout mice. Oral administration of Bifidobacterium longum subsp. infantis containing the IA-producing fldI gene prevents NEC in mice. Our study uncovers IA as a microbiota-derived therapeutic inhibiting STAT1-driven necroptosis via the AhR-SOCS5 axis, offering a targeted strategy for NEC management.

Indexed as

Enterocolitis, NecrotizingGastrointestinal MicrobiomeIndolesIntestinal MucosaNecroptosisAnimalsAnimals, NewbornBasic Helix-Loop-Helix ProteinsDisease Models, AnimalEpithelial CellsHumansInfant, NewbornMiceMice, Inbred C57BLMice, KnockoutReceptors, Aryl HydrocarbonBasic Helix-Loop-Helix ProteinsIndolesReceptors, Aryl HydrocarbonSTAT1 Transcription Factor3-indoleacrylic acidaryl hydrocarbon receptornecroptosisnecrotizing enterocolitis

Identifiers

PMID41923629
PMCPMC13130684

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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.