Evidence map›Paper›PMID 39520502›Full record

ArticleMetabolomics : Official journal of the Metabolomic Society2024

Regulation of ROS metabolism in macrophage via xanthine oxidase is associated with disease progression in pulmonary tuberculosis.

Ruichao Liu, Fuzhen Zhang, Shanshan Li, Qiuyue Liu, Yu Pang, Liang Li

Abstract read
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In one paragraph

Article in Metabolomics : Official journal of the Metabolomic Society, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

6 authors.

Ruichao Liu *Department of Bacteriology and Immunology, Beijing Tuberculosis & Thoracic Tumor Research Institute/Beijing Chest Hospital, Capital Medical University, Beijing, 101149, P.R. China.
Fuzhen Zhang *Department of Epidemiology, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan, 250012, P.R. China.
Shanshan LiDepartment of Bacteriology and Immunology, Beijing Tuberculosis & Thoracic Tumor Research Institute/Beijing Chest Hospital, Capital Medical University, Beijing, 101149, P.R. China.
Qiuyue LiuDepartment of Intensive Care Unit, Beijing Tuberculosis & Thoracic Tumor Research Institute/Beijing Chest Hospital, Capital Medical University, Beijing, 101149, P.R. China. liuqiuyue@bjxkyy.cn.
Yu PangDepartment of Bacteriology and Immunology, Beijing Tuberculosis & Thoracic Tumor Research Institute/Beijing Chest Hospital, Capital Medical University, Beijing, 101149, P.R. China. pangyupound@163.com.
Liang LiDepartment of Bacteriology and Immunology, Beijing Tuberculosis & Thoracic Tumor Research Institute/Beijing Chest Hospital, Capital Medical University, Beijing, 101149, P.R. China. liliang69@vip.sina.com.

Funding

Beijing Nova Program 20220484169Beijing Nova Program 20230484295National Key Research and Development Program of China 2022YFC2304803National Natural Science Foundation of China 82100011
6 · The paper itself

Abstract

backgroundPulmonary tuberculosis (PTB) exacerbation can lead to respiratory failure, multi-organ failure, and symptoms related to central nervous system diseases. The purpose of this study is to screen biomarkers and metabolic pathways that can predict the progression of PTB, and to verify the role of the metabolic enzyme xanthine oxidase (XO) in the progression of PTB.

methodsTo explore the biomarkers and mechanisms underlying the progression of PTB, plasma metabolomics sequencing was conducted on patients with severe PTB, non-severe PTB, and healthy individuals. Screening differential metabolites and metabolic pathways that can predict the progression of PTB, and verifying the function and mechanism of action of XO through experiments.

resultsThe purine metabolism, sphingolipid metabolism, and amino acid metabolism between the three groups differ. In patients with severe PTB, the levels of xanthosine and hypoxanthine are increased, while the levels of D-tryptophan, dihydroceramide and uric acid are decreased. Inhibition of XO activity has been observed to reduce the levels of tumor necrosis factor (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6), as well as to suppress the production of reactive oxygen species (ROS) and the activation of the NF-κB pathway, while also promoting the growth of MTB within cells.

conclusionD-tryptophan, xanthosine, and dihydroceramide can be utilized as biomarkers for progression of PTB, assisting in the evaluation of disease progression, and XO stands out as a potential therapeutic target for impeding the progression of PTB.

Indexed as

Disease ProgressionMacrophagesReactive Oxygen SpeciesTuberculosis, PulmonaryXanthine OxidaseAdultBiomarkersFemaleHumansMaleMetabolomicsBiomarkersReactive Oxygen SpeciesXanthine OxidaseBiomarkersDisease progressionPulmonary tuberculosisReactive oxygen speciesXanthine oxidase

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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.