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. 2021 Nov 30;16:1975–1986. doi: 10.2147/CIA.S339590

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© 2021 Huang et al.

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).

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The underlying mechanism of AF caused by TMAO. Created by ScienceSlides Software and Microsoft Office PowerPoint Software. Elevated plasma TMAO levels can promote AF in different ways. Firstly, activating NLRP3 inflammatory bodies and the NF-κ B pathway leads to the release of inflammatory factors and further promotes NGF expression. Both inflammatory factors and NGF can stimulate atrial plexus and induce AF. On the other hand, TMAO can activate the TGF-β1/Smad3 signaling pathway, and the activated inflammatory factors further promote myocardial fibrosis and induce arrhythmia.

Abbreviations: TMA, trimethylamine; FMOs, flavin-containing monooxygenases; NGF, nerve growth factor; +, elevated.