Evidence map›Paper›PMID 40378019›Full record

ArticleAging2025

The aspartate superpathway in gut microbiota-related metabolic pathways mediates immune cell protection against COPD and IPF: a Mendelian randomization analysis.

Lei Chen, Haoyan Chen, Qin Li, Jun Ma, Yanzhi Feng, Shenghua Zhang, Yu Han, Jie Pan, Mingjiong Zhang, Kai Sun and 1 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–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

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Research advance in correlation between childhood asthma and gut microbiota.Frontiers in cellular and infection microbiology · 2025
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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

11 authors.

Lei ChenDepartment of Geriatrics, Jiangsu Key Laboratory of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Haoyan ChenDepartment of Geriatrics, Jiangsu Key Laboratory of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Qin LiCenter of Molecular and Cellular Oncology, Yale School of Medicine, New Haven, CT 06510, USA.
Jun MaDepartment of Respiratory Medicine, Affiliated Nantong Hospital of Shanghai University (The Sixth People’s Hospital of Nantong), Nantong, China.
Yanzhi FengCenter of Molecular and Cellular Oncology, Yale School of Medicine, New Haven, CT 06510, USA.
Shenghua ZhangThe First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yu HanDepartment of Geriatrics, Jiangsu Key Laboratory of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Jie PanDepartment of Rheumatology and Immunology, Liyang Branch of Jiangsu Province Hospital, Liyang, China.
Mingjiong ZhangDepartment of Geriatrics, Jiangsu Key Laboratory of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Kai SunDepartment of Geriatrics, Jiangsu Key Laboratory of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Shuangshuang WuDepartment of Geriatrics, Jiangsu Key Laboratory of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBoth genetic and environmental factors can influence idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD) development. The gut microbiota plays crucial roles in maintaining tissue homeostasis. Dysregulation of the gut microbiota can result in disease. However, whether the alteration of the gut microbiota influences IPF and COPD remains unknown. RESEARCH QUESTION: What is the causal relationship between IPF, COPD and the gut microbiota-related metabolic pathways? What are the potential intermediate mediators in this relationship? STUDY DESIGN AND

methodsIntersect the gut microbiota and its metabolic pathways associated with IPF and COPD. Utilizing summary data from GWAS in public databases, a two-sample Mendelian randomization (MR) analysis was conducted on the gut microbiota-related metabolic pathway, the aspartate superpathway, in relation to IPF and COPD. Furthermore, we employed a two-step MR to quantify the proportion of influence mediated by monocytes and cDCs on the aspartate superpathway in relation to IPF and COPD.

resultsThe MR analysis found that the aspartate superpathway decreased the risk of developing IPF and COPD. Monocytes and cDCs acted as intermediary substances, participating in this with influence proportions of 7.88% and 6.27%, respectively.

interpretationThere is a causal link between the gut microbiota-related metabolic pathway, the aspartate superpathway, and IPF and COPD, where the influence is partially mediated by monocytes and cDCs. In clinical practice, we increase the focus on gut microbiota-mediated immune cells in relation to IPF and COPD.

Indexed as

Aspartic AcidGastrointestinal MicrobiomeIdiopathic Pulmonary FibrosisMetabolic Networks and PathwaysPulmonary Disease, Chronic ObstructiveGenome-Wide Association StudyHumansMendelian Randomization AnalysisMonocytesAspartic Acidchronic obstructive pulmonary disease (COPD)gut microbiotaidiopathic pulmonary fibrosis (IPF)immune cellsMendelian randomization

Identifiers

PMID40378019
PMCPMC12151505

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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.