Evidence map›Paper›PMID 39180691›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2024

RIP3 regulates doxorubicin-induced intestinal mucositis via FUT2-mediated α-1,2-fucosylation.

Wei Wen, Xiaomin Hu, Jialin Liu, Fanxin Zeng, Yihua Xu, Ye Yuan, Chunyan Gao, Xueting Sun, Bo Cheng, Jue Wang and 4 more

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

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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

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

14 authors.

Wei Wen *Institute of Molecular Medicine, College of Future Technology, Peking University, Beijing, 100871, China.
Xiaomin Hu *Institute of Molecular Medicine, College of Future Technology, Peking University, Beijing, 100871, China.
Jialin Liu *College of Chemistry and Molecular Engineering, Peking University, Beijing, 100871, China.
Fanxin Zeng *Institute of Molecular Medicine, College of Future Technology, Peking University, Beijing, 100871, China.
Yihua Xu *Institute of Molecular Medicine, College of Future Technology, Peking University, Beijing, 100871, China.
Ye YuanInstitute of Molecular Medicine, College of Future Technology, Peking University, Beijing, 100871, China.
Chunyan GaoInstitute of Molecular Medicine, College of Future Technology, Peking University, Beijing, 100871, China.
Xueting SunInstitute of Molecular Medicine, College of Future Technology, Peking University, Beijing, 100871, China.
Bo ChengCollege of Chemistry and Molecular Engineering, Peking University, Beijing, 100871, China.
Jue WangInstitute of Molecular Medicine, College of Future Technology, Peking University, Beijing, 100871, China.
Xinli HuInstitute of Molecular Medicine, College of Future Technology, Peking University, Beijing, 100871, China.
Rui-Ping XiaoInstitute of Molecular Medicine, College of Future Technology, Peking University, Beijing, 100871, China. xiaor@pku.edu.cn.
Xing ChenCollege of Chemistry and Molecular Engineering, Peking University, Beijing, 100871, China. xingchen@pku.edu.cn.
Xiuqin ZhangInstitute of Molecular Medicine, College of Future Technology, Peking University, Beijing, 100871, China. zhangxq@pku.edu.cn.

Funding

National High Level Hospital Clinical Research Funding 2022-PUMCH-A-026National Key Research and Development Program of China 2018YFA0801403
6 · The paper itself

Abstract

objectiveIntestinal mucositis is one of the common side effects of anti-cancer chemotherapy. However, the molecular mechanisms involved in mucositis development remain incompletely understood. In this study, we investigated the function of receptor-interacting protein kinase 3 (RIP3/RIPK3) in regulating doxorubicin-induced intestinal mucositis and its potential mechanisms.

methodsIntestinal mucositis animal models were induced in mice for in vivo studies. Rat intestinal cell line IEC-6 was used for in vitro studies. RNA‑seq was used to explore the transcriptomic changes in doxorubicin-induced intestinal mucositis. Intact glycopeptide characterization using mass spectrometry was applied to identify α-1,2-fucosylated proteins associated with mucositis.

resultsDoxorubicin treatment increased RIP3 expression in the intestine and caused severe intestinal mucositis in the mice, depletion of RIP3 abolished doxorubicin-induced intestinal mucositis. RIP3-mediated doxorubicin-induced mucositis did not depend on mixed lineage kinase domain-like (MLKL) but on α-1,2-fucosyltransferase 2 (FUT2)-catalyzed α-1,2-fucosylation on inflammation-related proteins. Deficiency of MLKL did not affect intestinal mucositis, whereas inhibition of α-1,2-fucosylation by 2-deoxy-D-galactose (2dGal) profoundly attenuated doxorubicin-induced inflammation and mucositis.

conclusionsRIP3-FUT2 pathway is a central node in doxorubicin-induced intestinal mucositis. Targeting intestinal RIP3 and/or FUT2-mediated α-1,2-fucosylation may provide potential targets for preventing chemotherapy-induced intestinal mucositis.

Indexed as

DoxorubicinFucosyltransferasesGalactoside 2-alpha-L-fucosyltransferaseMice, Inbred C57BLMucositisReceptor-Interacting Protein Serine-Threonine KinasesAnimalsAntibiotics, AntineoplasticCell LineIntestinal MucosaMaleMiceMice, KnockoutRatsAntibiotics, AntineoplasticDoxorubicinFucosyltransferasesGalactoside 2-alpha-L-fucosyltransferaseReceptor-Interacting Protein Serine-Threonine KinasesRipk3 protein, mouseDoxorubicinFUT2Intestinal mucositisRIP3Α-1,2-fucosylation

Identifiers

PMID39180691

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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.