Evidence map›Paper›PMID 40863120›Full record

ArticleMetabolites2025

The Causal Role of the Gut Microbiota-Plasma Metabolome Axis in Myeloproliferative Neoplasm Pathogenesis: A Mendelian Randomization and Mediation Analysis.

Hao Kan, Ka Zhang, Aiqin Mao, Li Geng

Abstract read
In one paragraph

Article in Metabolites, 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

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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

Who cites it

3 citing papers in PubMed.

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4 · The record

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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

4 authors.

Hao KanWuxi School of Medicine, Jiangnan University, Wuxi 214125, China.
Ka ZhangWuxi School of Medicine, Jiangnan University, Wuxi 214125, China.
Aiqin MaoWuxi School of Medicine, Jiangnan University, Wuxi 214125, China.
Li GengWuxi School of Medicine, Jiangnan University, Wuxi 214125, China.

Funding

Natural Science Foundation of Jiangsu Province BK20241621Postdoctoral Fellowship Program of CPSF GZC20230981
6 · The paper itself

Abstract

backgroundMyeloproliferative neoplasms (MPN), a group of chronic hematologic neoplasms, are driven by inflammatory mechanisms that influence disease initiation and progression. Emerging evidence highlights the gut microbiome and plasma metabolome as pivotal immunomodulators, yet their causal roles in MPN pathogenesis remain uncharacterized.

methodsWe conducted a two-sample Mendelian randomization (MR) analysis to systematically evaluate causal relationships between 196 gut microbial taxa, 526 plasma metabolites, and MPN risk. Instrumental variables were derived from genome-wide association studies (GWASs) of microbial/metabolite traits. Validation utilized 16S rRNA sequencing data from NCBI Bioproject PRJNA376506. Mediation and multivariable MR analyses elucidated metabolite-mediated pathways linking microbial taxa to MPN.

resultsOur MR analysis revealed that 7 intestinal taxa and 17 plasma metabolites are causally linked to MPN. External validation confirmed the three taxa's differential abundance in MPN cohorts. Mediation analysis revealed two mediated relationships, of which succinylcarnitine mediated 14.5% of the effect, and lysine 27.9%, linking the

conclusionsThis study identifies novel gut microbiota-metabolite axes driving MPN pathogenesis through immunometabolic mechanisms. The validated biomarkers provide potential therapeutic targets for modulating inflammation in myeloproliferative disorders.

Indexed as

gut microbiomemediation analysismendelian randomization analysismyeloproliferative neoplasmplasma metabolites

Identifiers

PMID40863120
PMCPMC12388087

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