2026-04-14T07:31:58Zhttps://recercat.cat/oai/request

oai:recercat.cat:2072/4671542026-03-28T08:31:03Zcom_2072_98col_2072_378192

Gut Microbiota-Derived TMAO : A Causal Factor Promoting Atherosclerotic Cardiovascular Disease? Canyelles, Marina Borràs, Carla Rotllan, Noemi Tondo Colomer, Mireia Escolà-Gil, Joan Carles Blanco Vaca, Francisco Universitat Autònoma de Barcelona Atherosclerosis TMAO Mortality CVD Renal function Prospective Altres ajuts: Red de Investigación en "Enfermedades Metabólicas y Cáncer", RED2018-102799-T ; FPU (Formación de Profesorado Universitario), FPU20/07440 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. 2023 Article de revisió https://ddd.uab.cat/record/273352 urn:10.3390/ijms24031940 urn:oai:ddd.uab.cat:273352 urn:articleid:14220067v24 urn:pmcid:PMC9916030 urn:pmc-uid:9916030 urn:pmid:36768264 urn:oai:pubmedcentral.nih.gov:9916030 urn:oai:egreta.uab.cat:publications/dfc229c2-be23-41cc-ad1a-c5121a67c9d7 urn:scopus_id:85147947980 eng Agencia Estatal de Investigación PID2019-104367RB-I00 Instituto de Salud Carlos III PI18-00164 Instituto de Salud Carlos III PI19-00136 Instituto de Salud Carlos III CM20/00033 International journal of molecular sciences ; Vol. 24 (january 2023) open access Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original. https://creativecommons.org/licenses/by/4.0/ application/pdf