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Published on: October 20, 2018
Trimethylamine N-Oxide Generated by the Gut Microbiota Is Associated with Vascular Inflammation: New Insights into
Yarong Liu1,2,3, Min Dai1,2,3
1School of Pharmacy, Anhui University of Chinese Medicine, Hefei, Anhui, China.
Abstract:
Trimethylamine N-oxide (TMAO) is a biologically active molecule generated by the gut microbiota. Accumulating evidences have indicated a close association between high plasma TMAO levels and the risk of developing atherosclerosis (AS). AS is considered a chronic inflammatory disease initiated by vascular endothelial inflammatory injury. Both observational and experimental studies suggest that TMAO can cause endothelial inflammatory injury. However, a clear mechanistic link between TMAO and vascular inflammation of AS is not yet summarized. In this review, we discuss the association between TMAO and AS and focus on the potential role of TMAO in endothelial inflammatory injury. Finally, the utility of TMAO-targeted therapeutic strategies for the treatment of AS is also analyzed.
Insights
Trimethylamine N-oxide (TMAO), a gut microbe byproduct, is linked to atherosclerosis (AS) risk. This review explores TMAO
Area of Science:
- Cardiovascular Biology
- Microbiome Research
- Inflammation Studies
Background:
- Trimethylamine N-oxide (TMAO) is a metabolite produced by gut microbiota.
- Elevated plasma TMAO levels are associated with increased risk of atherosclerosis (AS).
- AS is a chronic inflammatory condition involving vascular endothelial injury.
Purpose of the Study:
- To review the association between TMAO and AS.
- To elucidate the mechanistic link between TMAO and endothelial inflammation in AS.
- To analyze TMAO-targeted therapies for AS treatment.
Main Methods:
- Literature review of observational and experimental studies.
- Analysis of existing research on TMAO's role in vascular inflammation.
- Evaluation of potential therapeutic strategies targeting TMAO.
Main Results:
- Evidence suggests TMAO contributes to endothelial inflammatory injury.
- A clear mechanistic pathway linking TMAO to AS vascular inflammation is discussed.
- TMAO-targeted therapeutic approaches for AS are analyzed.
Conclusions:
- TMAO plays a significant role in the pathogenesis of AS via endothelial inflammation.
- Understanding TMAO's mechanisms is crucial for AS treatment.
- Targeting TMAO presents a potential therapeutic strategy for atherosclerosis.
