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REVIEW article

Front. Cell. Infect. Microbiol.

Sec. Intestinal Microbiome

Volume 15 - 2025 | doi: 10.3389/fcimb.2025.1488264

This article is part of the Research Topic The Role of Gut Microbes and Their Metabolites in Immune-related Diseases-Volume II View all 16 articles

The microbial metabolite trimethylamine N-oxide and the kidney diseases

Provisionally accepted
Jin-Qi Su Jin-Qi Su Xiang-Qi Wu Xiang-Qi Wu Qi Wang Qi Wang Bo-Yang Xie Bo-Yang Xie Cui-Yan Xiao Cui-Yan Xiao Hong-Yong Su Hong-Yong Su Ji-Xin Tang Ji-Xin Tang *Cui-Wei Yao Cui-Wei Yao
  • Guangdong Medical University, Zhanjiang, China

The final, formatted version of the article will be published soon.

    Trimethylamine N-oxide (TMAO) is a metabolite produced by the gut microbiota from choline, phosphatidylcholine, and carnitine.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.

    Keywords: gut microbiome, TMAO, kidney injury, Chronic Kidney Disease, end-stage renal disease, Inflammatory mechanisms

    Received: 29 Aug 2024; Accepted: 24 Feb 2025.

    Copyright: © 2025 Su, Wu, Wang, Xie, Xiao, Su, Tang and Yao. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Ji-Xin Tang, Guangdong Medical University, Zhanjiang, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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