Evidence map›Paper›PMID 37691112›Full record

ArticleCell proliferation2024

Neutrophil extracellular traps aggravate intestinal epithelial necroptosis in ischaemia-reperfusion by regulating TLR4/RIPK3/FUNDC1-required mitophagy.

Chengnan Chu, Xinyu Wang, Fang Chen, Chao Yang, Lin Shi, Weiqi Xu, Kai Wang, Baochen Liu, Chenyang Wang, Dongping Sun and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell proliferation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.6field-weighted citation impact, top 4% of its field
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

35 citing papers in PubMed, 34 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Chengnan ChuDivision of Trauma and Acute Care Surgery, Department of Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu Province, China.ORCID https://orcid.org/0000-0001-9986-3508
Xinyu WangDivision of Trauma and Acute Care Surgery, Department of Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu Province, China.ORCID https://orcid.org/0000-0002-7605-3091
Fang ChenDivision of Trauma and Acute Care Surgery, Jinling Hospital, School of Medicine, Southeast University, Nanjing, Jiangsu Province, China.ORCID https://orcid.org/0000-0003-0186-6108
Chao YangDivision of Trauma and Acute Care Surgery, Department of Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu Province, China.
Lin ShiInstitute of Chemicobiology and Functional Materials, School of Chemistry and Chemical Engineering, Nanjing University of Science and Technology, Nanjing, Jiangsu Province, China.
Weiqi XuDivision of Trauma and Acute Care Surgery, Department of Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu Province, China.
Kai WangDivision of Trauma and Acute Care Surgery, Department of Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu Province, China.
Baochen LiuDivision of Trauma and Acute Care Surgery, Department of Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu Province, China.
Chenyang WangKey Laboratory of Intestinal Injury, Research Institute of General Surgery, Affiliated Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu, China.
Dongping SunInstitute of Chemicobiology and Functional Materials, School of Chemistry and Chemical Engineering, Nanjing University of Science and Technology, Nanjing, Jiangsu Province, China.
Jieshou LiDivision of Trauma and Acute Care Surgery, Department of Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu Province, China.
Weiwei DingDivision of Trauma and Acute Care Surgery, Department of Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu Province, China.ORCID https://orcid.org/0000-0002-5026-689X
Nanjing General Hospital of Nanjing Military Command · CNNanjing University of Science and Technology · CN

Funding

National Natural Science Foundation of China 51873087National Natural Science Foundation of China 81770532National Natural Science Foundation of China 82270587the Innovation Platform of Clinical Medical Center of Jiangsu Province YXZXA2016006the Open Project of the State Key Laboratory of Trauma, Burn and Combined Injury, Third Military Medical University SKLKF202103
6 · The paper itself

Abstract

Neutrophil extracellular trap (NET) has been confirmed to be related to gut barrier injury during intestinal ischaemia-reperfusion (II/R). However, the specific molecular regulatory mechanism of NETs in II/R-induced intestinal barrier damage has yet to be fully elucidated. Here, we reported increased NETs infiltration accompanied by elevated inflammatory cytokines, cellular necroptosis and tight junction disruption in the intestine of human II/R patients. Meanwhile, NETs aggravated Caco-2 intestinal epithelial cell necroptosis, impairing the monolayer barrier in vitro. Moreover, Pad4-deficient mice were used further to validate the role of NETs in II/R-induced intestinal injury. In contrast, NET inhibition via Pad4 deficiency alleviated intestinal inflammation, attenuated cellular necroptosis, improved intestinal permeability, and enhanced tight junction protein expression. Notably, NETs prevented FUN14 domain-containing 1 (FUNDC1)-required mitophagy activation in intestinal epithelial cells, and stimulating mitophagy attenuated NET-associated mitochondrial dysfunction, cellular necroptosis, and intestinal damage. Mechanistically, silencing Toll-like receptor 4 (TLR4) or receptor-interacting protein kinase 3 (RIPK3) via shRNA relieved mitophagy limitation, restored mitochondrial function and reduced NET-induced necroptosis in Caco-2 cells, whereas this protective effect was reversed by TLR4 or RIPK3 overexpression. The regulation of TLR4/RIPK3/FUNDC1-required mitophagy by NETs can potentially induce intestinal epithelium necroptosis.

Indexed as

Extracellular TrapsReperfusion InjuryAnimalsCaco-2 CellsHumansIschemiaMembrane ProteinsMiceMitochondrial ProteinsMitophagyNecroptosisReceptor-Interacting Protein Serine-Threonine KinasesReperfusionToll-Like Receptor 4FUNDC1 protein, humanFUNDC1 protein, mouseMembrane ProteinsMitochondrial ProteinsReceptor-Interacting Protein Serine-Threonine KinasesRIPK3 protein, humanTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID37691112
PMCPMC10771116
OpenAlexW4386590508

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.