Literature DB >> 29425570

A potential relationship between gut microbes and atrial fibrillation: Trimethylamine N-oxide, a gut microbe-derived metabolite, facilitates the progression of atrial fibrillation.

Lilei Yu1, Guannan Meng1, Bing Huang1, Xiaoya Zhou1, Stavros Stavrakis2, Menglong Wang1, Xuefei Li1, Liping Zhou1, Yuhong Wang1, Meng Wang1, Zhenya Wang1, Jielin Deng1, Sunny S Po3, Hong Jiang4.   

Abstract

BACKGROUND: Emerging evidence indicates gut microbes and their products could activate the autonomic nervous system (ANS), which plays important roles in the initiation and maintenance of atrial fibrillation (AF). Trimethylamine N-oxide (TMAO), a metabolite derived from gut microbes, is associated with cardiovascular diseases. The present study aimed to investigate the role of TMAO in the progression of AF.
METHODS: In part 1: TMAO or saline was locally injected into 4 major atrial ganglionated plexi (GP) to clarify its effect on cardiac ANS and AF inducibility in normal canines. In part 2: TMAO or saline was injected into 4 major atrial GP to test its effect on AF progression in a rapid atrial pacing (RAP)-induced AF model.
RESULTS: In part 1: Local injection of TMAO significantly increased anterior right GP (ARGP) function and neural activity, shortened ERP values. In part 2, compared with the control group, 6-hour RAP significantly shortened the ERP, widened the ∑WOV, enhanced the ARGP function and neural activity, increased the NGF and c-fos expression, and up-regulated the inflammatory cytokines. TMAO aggravated all of these changes by activating the proinflammatory p65 NF-κB signaling pathway.
CONCLUSIONS: TMAO could increase the instability of atrial electrophysiology in normal canines and aggravate the acute electrical remodeling in a RAP-induced AF model by exacerbating autonomic remodeling. The increased inflammatory cytokines in the GP due to the activation of p65 NF-κB signaling may contribute to these effects.
Copyright © 2017 Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Atrial fibrillation; Autonomic nervous system; Gut microbes; Inflammation; Trimethylamine N-oxide

Mesh:

Substances:

Year:  2018        PMID: 29425570     DOI: 10.1016/j.ijcard.2017.11.071

Source DB:  PubMed          Journal:  Int J Cardiol        ISSN: 0167-5273            Impact factor:   4.164


  28 in total

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9.  Metagenomic data-mining reveals enrichment of trimethylamine-N-oxide synthesis in gut microbiome in atrial fibrillation patients.

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10.  Gut-microbiota derived TMAO: A risk factor, a mediator or a bystander in the pathogenesis of atrial fibrillation?

Authors:  Monika Gawałko; Dominik Linz; Dobromir Dobrev
Journal:  Int J Cardiol Heart Vasc       Date:  2021-06-15
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