ArticleInternational journal of molecular sciences2022
Trimethylamine N-Oxide (TMAO) Impairs Purinergic Induced Intracellular Calcium Increase and Nitric Oxide Release in Endothelial Cells.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Trimethylamine N-oxide (TMAO) disrupts endothelial junction integrity through VE-cadherin Tyr658 phosphorylation in vitro.Archives of toxicology · 2026Article
- The Heart-Gut Axis in Heart Failure: The Role of Next-Generation Pharmacological Therapies.International journal of molecular sciences · 2026Review
- Dietary Nutrients, Gut Microbiota, and Cardiac Function: From Metabolic Mechanisms to Clinical Applications.Nutrients · 2026Review
- Microbiota-Mediated Crosstalk Between the Gut and the Vascular System: Protective Effects of Novel Postbiotic Formulations on Human Endothelial and Vascular Smooth Muscle Cells.International journal of molecular sciences · 2026Article
- Trimethylamine-Annals of medicine · 2025Review
- From Gut to Heart: Targeting Trimethylamine N-Oxide as a Novel Strategy in Heart Failure Management.Biomolecules · 2025Review
- The gut-heart axis: a correlation between Paneth cells' dysfunction, microbiome dysbiosis, and cardiovascular diseases.Cell communication and signaling : CCS · 2025Review
- Trimethylamine N-Oxide (TMAO) Acts as Inhibitor of Endothelial Nitric Oxide Synthase (eNOS) and Hampers NO Production and Acetylcholine-Mediated Vasorelaxation in Rat Aortas.Antioxidants (Basel, Switzerland) · 2025Article
- The gut microbiota metabolite trimethylamine N-oxide promotes cardiac hypertrophy by activating the autophagic degradation of SERCA2a.Communications biology · 2025Article
- The gut microbiota in thrombosis.Nature reviews. Cardiology · 2025Review
- Purinergic signaling in the battlefield of viral infections.Purinergic signalling · 2025Review
- The bidirectional regulatory mechanism of gut microbiota metabolites on myocardial injury in heart failure from the perspective of the gut-heart axis: a review.Frontiers in microbiology · 2025Review
- The microbial metabolite trimethylamine N-oxide and the kidney diseases.Frontiers in cellular and infection microbiology · 2025Review
- Angiogenesis, a key point in the association of gut microbiota and its metabolites with disease.European journal of medical research · 2024Review
- Low-Molecular-Weight Compounds Produced by the Intestinal Microbiota and Cardiovascular Disease.International journal of molecular sciences · 2024Review
- Trimethylamine-N-oxide promotes osteoclast differentiation and oxidative stress by activating NF-κB pathway.Aging · 2024Article
- The gut microbiome as a modulator of arterial function and age-related arterial dysfunction.American journal of physiology. Heart and circulatory physiology · 2024Review
- Research progress in the relationship between gut microbiota metabolite trimethylamine N-oxide and ischemic stroke.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- Indole-3-Propionic Acid, a Gut Microbiota-Derived Tryptophan Metabolite, Promotes Endothelial Dysfunction Impairing Purinergic-Induced Nitric Oxide Release in Endothelial Cells.International journal of molecular sciences · 2024Article
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Authors and funding
5 authors.
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Abstract
Trimethylamine N-oxide (TMAO) is a diet derived compound directly introduced through foodstuff, or endogenously synthesized from its precursors, primarily choline, L-carnitine, and ergothioneine. New evidence outlines high TMAO plasma concentrations in patients with overt cardiovascular disease, but its direct role in pathological development is still controversial. The purpose of the study was to evaluate the role of TMAO in affecting key intracellular factors involved in endothelial dysfunction development, such as reactive oxygen species, mitochondrial health, calcium balance, and nitric oxide release using bovine aortic endothelial cells (BAE-1). Cell viability and oxidative stress indicators were monitored after acute and prolonged TMAO treatment. The role of TMAO in interfering with the physiological purinergic vasodilatory mechanism after ATP stimulation was defined through measurements of the rise of intracellular calcium, nitric oxide release, and eNOS phosphorylation at Ser1179 (eNOS
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