Evidence map›Paper›PMID 36768264›Full record

ReviewInternational journal of molecular sciences2023

Gut Microbiota-Derived TMAO: A Causal Factor Promoting Atherosclerotic Cardiovascular Disease?

Marina Canyelles, Carla Borràs, Noemí Rotllan, Mireia Tondo, Joan Carles Escolà-Gil, Francisco Blanco-Vaca

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed, 7 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

127 citing papers in PubMed, 7 syntheses or guidelines pooled it.

  1. Pooled it
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  8. Trial
  9. Abnormal "Frontiers in cardiovascular medicine · 2026
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  12. Review
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  15. Glycyrrhizic Acid Alleviates Atherosclerosis inInternational journal of molecular sciences · 2026
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  19. Review
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67 more citing papers are in PubMed but not listed here.

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.

Marina CanyellesInstitut de Recerca de l'Hospital Santa Creu i Sant Pau, Institut d'Investigacions Biomèdiques IIB Sant Pau, 08041 Barcelona, Spain.ORCID 0000-0002-0278-5337
Carla BorràsInstitut de Recerca de l'Hospital Santa Creu i Sant Pau, Institut d'Investigacions Biomèdiques IIB Sant Pau, 08041 Barcelona, Spain.
Noemí RotllanInstitut de Recerca de l'Hospital Santa Creu i Sant Pau, Institut d'Investigacions Biomèdiques IIB Sant Pau, 08041 Barcelona, Spain.ORCID 0000-0002-0587-8045
Mireia TondoCIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), 28029 Madrid, Spain.ORCID 0000-0002-0301-9984
Joan Carles Escolà-GilInstitut de Recerca de l'Hospital Santa Creu i Sant Pau, Institut d'Investigacions Biomèdiques IIB Sant Pau, 08041 Barcelona, Spain.ORCID 0000-0001-9021-2485
Francisco Blanco-VacaCIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), 28029 Madrid, Spain.ORCID 0000-0001-7380-5385

Funding

Instituto de Salud Carlos III PI18-00164 and PI21-00140 (to F.B.-V. and M.T.)Instituto de Salud Carlos III PI19-00136 (to J.C.E-G)Instituto de Salud Carlos III Rio Hortega contract CM20/00033Ministry of Economy, Industry and Competitiveness FPU20/07440Ministry of Economy, Industry and Competitiveness PID2019-104367RB-100 to N.RMinistry of Economy, Industry and Competitiveness RED2018-102799-T
6 · The paper itself

Abstract

Trimethylamine-N-oxide (TMAO) is the main diet-induced metabolite produced by the gut microbiota, and it is mainly eliminated through renal excretion. TMAO has been correlated with an increased risk of atherosclerotic cardiovascular disease (ASCVD) and related complications, such as cardiovascular mortality or major adverse cardiovascular events (MACE). Meta-analyses have postulated that high circulating TMAO levels are associated with an increased risk of cardiovascular events and all-cause mortality, but the link between TMAO and CVD remains not fully consistent. The results of prospective studies vary depending on the target population and the outcome studied, and the adjustment for renal function tends to decrease or reverse the significant association between TMAO and the outcome studied, strongly suggesting that the association is substantially mediated by renal function. Importantly, one Mendelian randomization study did not find a significant association between genetically predicted higher TMAO levels and cardiometabolic disease, but another found a positive causal relationship between TMAO levels and systolic blood pressure, which-at least in part-could explain the link with renal function. The mechanisms by which TMAO can increase this risk are not clearly elucidated, but current evidence indicates that TMAO induces cholesterol metabolism alterations, inflammation, endothelial dysfunction, and platelet activation. Overall, there is no fully conclusive evidence that TMAO is a causal factor of ASCVD, and, especially, whether TMAO induces or just is a marker of hypertension and renal dysfunction requires further study.

Indexed as

AtherosclerosisCardiovascular DiseasesGastrointestinal MicrobiomeHumansMethylaminesProspective StudiesMethylaminestrimethyloxamineatherosclerosisCVDmortalityprospectiverenal functionTMAO

Identifiers

PMID36768264
PMCPMC9916030

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.