ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2017
Trimethylamine-N-Oxide Instigates NLRP3 Inflammasome Activation and Endothelial Dysfunction.
Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers, 5 of them syntheses that pooled it.
What it found
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Who cites it
173 citing papers in PubMed, 5 syntheses or guidelines pooled it, 285 citations in OpenAlex.
- Gut microbiota-derived trimethylamine N-oxide is associated with the risk of all-cause and cardiovascular mortality in patients with chronic kidney disease: a systematic review and dose-response meta-analysis.Annals of medicine · 2023Pooled it
- Gut microbiota-derived metabolite trimethylamine-N-oxide and stroke outcome: a systematic review.Frontiers in molecular neuroscience · 2023Pooled it
- Gut microbiota-associated metabolite trimethylamine N-Oxide and the risk of stroke: a systematic review and dose-response meta-analysis.Nutrition journal · 2020Pooled it
- Trimethylamine-N-oxide has prognostic value in coronary heart disease: a meta-analysis and dose-response analysis.BMC cardiovascular disorders · 2020Pooled it
- The Gut Microbial Metabolite Trimethylamine N-Oxide and Hypertension Risk: A Systematic Review and Dose-Response Meta-analysis.Advances in nutrition (Bethesda, Md.) · 2020Pooled it
- Modulation of the response to immunotherapy in triple-negative breast cancer: the role of the microbiota and microbial metabolites in the tumor microenvironment.Gut microbes · 2026Review
- Targeting FMO3 suppresses the malignant phenotype of colorectal cancer: evidence from bioinformatics to functional experiments.Future science OA · 2026Article
- Gut-heart-kidney communication in cardiovascular disease: from a single-metabolite hypothesis to a context-dependent metabolite network.American journal of physiology. Heart and circulatory physiology · 2026Review
- Gut‑liver‑kidney axis: A systems biology framework for understanding and treating chronic kidney disease (Review).International journal of molecular medicine · 2026Review
- Cognitive-Motor Dual Task Training Synergistically Improves Aging-related Cognitive Dysfunction By Reducing TMAO and Suppressing TXNIP/NLRP3 Pathway.Molecular neurobiology · 2026Article
- Gut microecology and cardiovascular disease: core pathogenic mechanisms and clinical intervention strategies.Folia microbiologica · 2026Review
- Membrane Raft Redox Signaling Mediates Trimethylamine N-Oxide-Induced NLRP3 Inflammasome Activation and Endothelial Dysfunction.Antioxidants (Basel, Switzerland) · 2026Article
- Trimethylamine N-oxide and Homocysteine in Kidney Function and Disease: Distinct Metabolic Origins, Shared Renal Determinants and Pathophysiological Pathways.International journal of molecular sciences · 2026Review
- Gut microbiota-atrium axis: Microbiota metabolite-mediated regulation of the NLRP3 inflammasome in atrial fibrillation-pathophysiological roles and therapeutic perspectives.Heart rhythm O2 · 2026Review
- Cardioprotective Effects of Ling-Gui-Zhu-Gan Decoction Against Ventricular Remodeling after Acute Myocardial Infarction via ROS/TXNIP/NLRP3 Signaling.Chinese journal of integrative medicine · 2026Article
- Associations of trimethylamine N-oxide and its precursors with hypertensive disorders of pregnancy, its subtypes and blood pressure in the offspring: findings from the Shanghai Birth Cohort.BMC pregnancy and childbirth · 2026Article
- Senescent cells in systemic aging: SASP heterogeneity, immune escape, and endocrine modulation.Biogerontology · 2026Review
- Translating microbial dysbiosis into brain health interventions: a focus on the oral-gut-reproductive inflammatory pathways.Archives of microbiology · 2026Review
- Article
- Multi-Omics Mechanisms of Trimethylamine Oxide and Cardiovascular Disease: A Review.Reviews in cardiovascular medicine · 2026Review
113 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND/
aimPlasma trimethylamine-N-oxide (TMAO), a product of intestinal microbial metabolism of dietary phosphatidylcholine has been recently associated with atherosclerosis and increased risk of cardiovascular diseases (CVD) in rodents and humans. However, the molecular mechanisms of how TMAO induces atherosclerosis and CVD progression are still unclear. The present study tested whether TMAO induces NLRP3 inflammasome formation and activation and thereby contributes to endothelial injury initiating atherogenesis.
methodsInflammasome formation and activation was determined by confocal microscopy, caspase-1 activity was measured by colorimetric assay, IL-1β production was measured using ELISA, cell permeability was determined by microplate reader and ZO-1 expression was determined by western blot analysis and confocal microscopy. In in vivo experiments, TMAO was infused by osmotic pump implantation.
resultsTMAO treatment significantly increased the colocalization of NLRP3 with Asc or NLRP3 with caspase-1, caspase-1 activity, IL-1β production, cell permeability in carotid artery endothelial cells (CAECs) compared to control cells. Pretreatment with caspase-1 inhibitor, WEHD or Nlrp3 siRNA abolished the TMAO-induced inflammasome formation, activation and cell permeability in these cells. In addition, we explored the mechanisms by which TMAO activates NLRP3 inflammasomes. TMAO-induced the activation of NLRP3 inflammasomes was associated with both redox regulation and lysosomal dysfunction. In animal experiments, direct infusion of TMAO in mice with partially ligated carotid artery were found to have increased NLRP3 inflammasome formation and IL-1β production in the intima of wild type mice.
conclusionThe formation and activation of NLRP3 inflammasomes by TMAO may be an important initiating mechanism to turn on the endothelial inflammatory response leading to endothelial dysfunction.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.