Evidence map›Paper›PMID 40926018›Full record

ArticleCellular & molecular immunology2025

Intestinal taurine acts as a novel immunometabolic modulator of IBD by degrading redundant mitochondrial RNA.

Le-Xi Wu, Jia-Huan Xie, Jie-Yu Li, Wen-Ping Li, Xin-Tao Mao, Ling-Jie Huang, Hao-Tian Chen, Jiang-Yan Zhong, Li-Min Lin, Shicheng Su and 3 more

Abstract read
In one paragraph

Article in Cellular & molecular immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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.

Le-Xi Wu *Department of Gastroenterology, Sir Run Run Shaw Hospital, College of Medicine Zhejiang University, Hangzhou, China.
Jia-Huan Xie *Center for Neuroimmunology and Health Longevity, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Jie-Yu Li *The MOE Key Laboratory of Biosystems Homeostasis & Protection, Zhejiang Provincial Key Laboratory for Cancer Molecular Cell Biology, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang, China.
Wen-Ping LiCenter for Neuroimmunology and Health Longevity, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Xin-Tao MaoCenter for Neuroimmunology and Health Longevity, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Ling-Jie HuangDepartment of Gastroenterology, Sir Run Run Shaw Hospital, College of Medicine Zhejiang University, Hangzhou, China.
Hao-Tian ChenDepartment of Gastroenterology, Sir Run Run Shaw Hospital, College of Medicine Zhejiang University, Hangzhou, China.
Jiang-Yan ZhongDepartment of Gastroenterology, Sir Run Run Shaw Hospital, College of Medicine Zhejiang University, Hangzhou, China.
Li-Min LinCenter for Neuroimmunology and Health Longevity, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Shicheng SuGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
Yi-Yuan LiSchool of Life, Beijing Institute of Technology, Zhuhai Campus, Zhuhai, China. 103200067@seu.edu.cn.
Qian CaoDepartment of Gastroenterology, Sir Run Run Shaw Hospital, College of Medicine Zhejiang University, Hangzhou, China. caoq@zju.edu.cn.ORCID 0000-0001-7938-7532
Jin JinDepartment of Gastroenterology, Sir Run Run Shaw Hospital, College of Medicine Zhejiang University, Hangzhou, China. jjin4@zju.edu.cn.ORCID 0000-0001-7887-5972

Funding

China National Funds for Distinguished Young Scientists 82125016National Science Foundation of China | Key Programme 82230061
6 · The paper itself

Abstract

Anti-tumor necrosis factor (TNF) therapy for inflammatory bowel disease (IBD) is hampered by issues of nonresponse and resistance, highlighting the urgent need for alternative or complementary treatments. Our study revealed significant upregulation of taurine in the intestinal tissues of IBD patients, which was inversely related to the severity of the disease. A key discovery was that TNF directly induced taurine synthesis in intestinal epithelial cells and increased the production of angiogenin, a nuclease that degrades mitochondrial RNA, which is known to amplify inflammatory responses. By degrading mitochondrial RNA, angiogenin inhibits the inflammatory response in macrophages, suggesting a potent immune-modulatory role for taurine. This mechanism implies that taurine could serve as an adjunct to anti-TNF therapies, enhancing their efficacy and providing a novel strategy for the management of IBD and other chronic inflammatory diseases by harnessing the body's innate immune regulatory mechanisms.

Indexed as

Inflammatory Bowel DiseasesIntestinal MucosaMitochondriaRNA, MitochondrialTaurineAnimalsFemaleHumansMacrophagesMaleMiceRibonuclease, PancreaticTumor Necrosis Factor-alphaangiogeninRibonuclease, PancreaticRNA, MitochondrialTaurineTumor Necrosis Factor-alphaAngiogeninImmunomodulationInflammatory Bowel Disease (IBD)Mitochondrial RNA (mtRNA)Taurine

Identifiers

PMID40926018
PMCPMC12575716

What OpenQuestion holds

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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.