Trimethylamine N‐Oxide Promotes Vascular Inflammation Through Signaling of Mitogen‐Activated Protein Kinase and Nuclear Factor‐κB

By M. Seldin, Yonghong Meng, Hongxiu Qi, Weifei Zhu, Zeneng Wang, S. Hazen, Aldons J. Lusis, D. Shih. Journal of the American Heart Association : Cardiovascular and Cerebrovascular Disease, 2016

694 citations recorded by the source corpus.

The choline‐derived metabolite trimethylamine N‐oxide (TMAO) has been demonstrated to contribute to atherosclerosis and is associated with coronary artery disease risk.

Subfields: Molecular Biology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/94f98bfae58196b4f7fcba097f14cdef7b021964

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In Molecular Biology

1. S. Ghosh
2. Zahraa Al Bander
3. N. Naderpoor
4. Aya Mousa
5. M. Nitert
6. T. Postler

In Rheumatology

1. S. Ghosh
2. T. Postler

Citations in the corpus

• Gut microbial metabolite TMAO enhances platelet hyperreactivity and thrombosis risk (2016, neutral): “Also shown are known effects of the gut microbial TMAO pathway on CVD, including the recent demonstration of adverse ventricular remodeling and heart failure risk (Organ et al., 2015), and arterial endothelial cell activation in vivo (Seldin et al., 2016).”
• Understanding the Holobiont: How microbial metabolites affect human health and shape the immune system (2017, background): “Interestingly, a recent study found that TMAO induced the transcription of several genes encoding pro-inflammatory, atherosclerosis-promoting proteins in endothelial and smooth-muscle cells (but not peritoneal macrophages) through an unknown mechanism (Seldin et al., 2016).”
• The Gut Microbiota and Inflammation: An Overview (2020, background): “[118] found that increased serum levels of TMAO induced a rise in the production of IL-6 and TNF-α by the NF-κB signalling pathway in mouse and human cell cultures.”