Evidence map›Paper›PMID 40134790›Full record

ReviewFrontiers in cellular and infection microbiology2025

The microbial metabolite trimethylamine N-oxide and the kidney diseases.

Jin-Qi Su, Xiang-Qi Wu, Qi Wang, Bo-Yang Xie, Cui-Yan Xiao, Hong-Yong Su, Ji-Xin Tang, Cui-Wei Yao

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in cellular and infection microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

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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

8 authors.

Jin-Qi SuGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Xiang-Qi WuGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Qi WangGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Bo-Yang XieGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Cui-Yan XiaoGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Hong-Yong SuGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Ji-Xin TangGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Cui-Wei YaoGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Trimethylamine N-oxide (TMAO), a metabolite, is a co-metabolite produced by both gut microbiota and livers, originating from foods rich in choline or carnitine. Emerging evidence suggests that TMAO may play a role in the pathogenesis of various kidney diseases, including acute kidney injury and chronic kidney disease. Research has demonstrated that heightened levels of TMAO are correlated with a heightened likelihood of kidney disease advancement and cardiovascular incidents among individuals with chronic kidney disease. Furthermore, TMAO has been observed to stimulate inflammation, oxidative stress, and fibrosis in animal models of kidney disease. Mechanistically, TMAO may contribute to kidney disease pathogenesis by inhibiting autophagy, activating the NLRP3 inflammasome, and inducing mitochondrial dysfunction. Therefore, targeting TMAO may represent a promising therapeutic strategy for the treatment of kidney diseases. Future studies are needed to further investigate the role of TMAO in kidney disease pathogenesis and to develop TMAO-targeted therapies for the prevention and treatment of kidney diseases.

Indexed as

Kidney DiseasesMethylaminesAcute Kidney InjuryAnimalsAutophagyDisease Models, AnimalGastrointestinal MicrobiomeHumansInflammasomesInflammationKidneyNLR Family, Pyrin Domain-Containing 3 ProteinOxidative StressRenal Insufficiency, ChronicInflammasomesMethylaminesNLR Family, Pyrin Domain-Containing 3 Proteintrimethyloxaminechronic kidney diseaseend-stage renal diseasegut microbiomeinflammatory mechanismskidney injuryTMAO

Identifiers

PMID40134790
PMCPMC11933022

What Socratic holds

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Registered trials

None linked

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 Socratic graph.