Evidence map›Paper›PMID 38773142›Full record

ArticleNature communications2024

Disruption of TIGAR-TAK1 alleviates immunopathology in a murine model of sepsis.

Dongdong Wang, Yanxia Li, Hao Yang, Xiaoqi Shen, Xiaolin Shi, Chenyu Li, Yongjing Zhang, Xiaoyu Liu, Bin Jiang, Xudong Zhu and 9 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Review
  2. Article
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  5. Article
  6. Article
  7. Review
  8. OralWorld journal of diabetes · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

19 authors.

Dongdong Wang *Department of Pathophysiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.
Yanxia Li *Department of Pathophysiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.
Hao Yang *School of Life Science and Technology, and Shanghai Institute for Advanced Immunochemical Studies, ShanghaiTech University, Shanghai, China.ORCID http://orcid.org/0009-0008-0040-276X
Xiaoqi ShenDepartment of Pathophysiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.
Xiaolin ShiDepartment of Pathophysiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.
Chenyu LiDepartment of Pathophysiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.
Yongjing ZhangDepartment of Pathophysiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.
Xiaoyu LiuJiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, China.
Bin JiangDepartment of Pathophysiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.
Xudong ZhuDepartment of Pathophysiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.
Hanwen ZhangDepartment of Pathophysiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.ORCID http://orcid.org/0000-0002-7855-2564
Xiaoyu LiDepartment of Pathophysiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.
Hui BaiDepartment of Pathophysiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.
Qing YangDepartment of Pathophysiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.
Wei GaoThe Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou Medical Center, Nanjing Medical University, Nanjing, China.ORCID http://orcid.org/0000-0002-7889-1662
Fang BaiSchool of Life Science and Technology, and Shanghai Institute for Advanced Immunochemical Studies, ShanghaiTech University, Shanghai, China.ORCID http://orcid.org/0000-0003-1468-5568
Yong JiDepartment of Pathophysiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.ORCID http://orcid.org/0000-0003-2650-5747
Qi ChenDepartment of Pathophysiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China. qichen@njmu.edu.cn.ORCID http://orcid.org/0000-0002-5289-4910
Jingjing BenDepartment of Pathophysiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China. bjj@njmu.edu.cn.ORCID http://orcid.org/0000-0002-2239-0105

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81830011National Natural Science Foundation of China (National Science Foundation of China) 82100433National Natural Science Foundation of China (National Science Foundation of China) 82300515
6 · The paper itself

Abstract

Macrophage-orchestrated inflammation contributes to multiple diseases including sepsis. However, the underlying mechanisms remain to be defined clearly. Here, we show that macrophage TP53-induced glycolysis and apoptosis regulator (TIGAR) is up-regulated in murine sepsis models. When myeloid Tigar is ablated, sepsis induced by either lipopolysaccharide treatment or cecal ligation puncture in male mice is attenuated via inflammation inhibition. Mechanistic characterizations indicate that TIGAR directly binds to transforming growth factor β-activated kinase (TAK1) and promotes tumor necrosis factor receptor-associated factor 6-mediated ubiquitination and auto-phosphorylation of TAK1, in which residues 152-161 of TIGAR constitute crucial motif independent of its phosphatase activity. Interference with the binding of TIGAR to TAK1 by 5Z-7-oxozeaenol exhibits therapeutic effects in male murine model of sepsis. These findings demonstrate a non-canonical function of macrophage TIGAR in promoting inflammation, and confer a potential therapeutic target for sepsis by disruption of TIGAR-TAK1 interaction.

Indexed as

Apoptosis Regulatory ProteinsDisease Models, AnimalLipopolysaccharidesMacrophagesMAP Kinase Kinase KinasesSepsisAnimalsHumansInflammationLactonesMaleMAP Kinase Kinase Kinase 7MiceMice, Inbred C57BLMice, KnockoutPhosphoric Monoester Hydrolases7-oxozeanolApoptosis Regulatory ProteinsLactonesLipopolysaccharidesMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesPhosphoric Monoester HydrolasesResorcinolsTIGAR protein, mouseTNF Receptor-Associated Factor 6Zearalenone

Identifiers

PMID38773142
PMCPMC11109194

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.