ArticleScientific reports2018
Contribution of multidrug and toxin extrusion protein 1 (MATE1) to renal secretion of trimethylamine-N-oxide (TMAO).
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Effects of SGLT-2 Inhibitors on Plasma Concentrations and Renal Clearance of the Risk Marker Trimethylamine-N-Oxide in Patients With Type-2 Diabetes.Endocrinology, diabetes & metabolism · 2026Trial
- 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
- Article
- Putative new biomarkers for renal transporter-mediated drug-drug interactions: Characterization as substrates of organic cation transporter 2, multidrug and toxin extrusion protein 1, and other important drug transporters.Drug metabolism and disposition: the biological fate of chemicals · 2025Article
- Urea, TMAO, betaine and other osmolytes as endogenous diuretics in heart failure and hypertension.Heart failure reviews · 2025Review
- Role of Transport Proteins for the Renal Handling of L-Arginine and Related Derivatives.International journal of molecular sciences · 2025Review
- Transport of the uremic toxin symmetric dimethylarginine (SDMA) by renal transport proteins.Amino acids · 2025Article
- Beyond ADME: The Endogenous Functions of Drug Transporters and Its Impact on Human Disease.Pharmaceutics · 2025Review
- Differential Analysis of Key Proteins Related to Fibrosis and Inflammation in Soluble Egg Antigen ofPathogens (Basel, Switzerland) · 2023Article
- Monosodium glutamate consumption reduces the renal excretion of trimethylamine N-oxide and the abundance of Akkermansia muciniphila in the gut.Biochemical and biophysical research communications · 2022Article
- MATE1 Deficiency Exacerbates Dofetilide-Induced Proarrhythmia.International journal of molecular sciences · 2022Article
- Trimethylamine N-Oxide (TMAO) Impairs Purinergic Induced Intracellular Calcium Increase and Nitric Oxide Release in Endothelial Cells.International journal of molecular sciences · 2022Article
- The Interplay between Uremic Toxins and Albumin, Membrane Transporters and Drug Interaction.Toxins · 2022Review
- The Accumulation and Molecular Effects of Trimethylamine N-Oxide on Metabolic Tissues: It's Not All Bad.Nutrients · 2021Review
- Phosphate, Microbiota and CKD.Nutrients · 2021Review
- Elevation of Trimethylamine-N-Oxide in Chronic Kidney Disease: Contribution of Decreased Glomerular Filtration Rate.Toxins · 2019Article
- Review
- Blood-brain barrier transporters: a translational consideration for CNS delivery of neurotherapeutics.Expert opinion on drug deliveryReview
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trimethylamine-N-oxide (TMAO) gained considerable attention because of its role as a cardiovascular risk biomarker. Organic cation transporter 2 (OCT2) mediates TMAO uptake into renal proximal tubular cells. Here we investigated the potential role of multidrug and toxin extrusion protein 1 (MATE1) for translocation of TMAO across the luminal membrane of proximal tubular cells. HEK293 cells stably expressing OCT2 (HEK-OCT2) or MATE1 (HEK-MATE1) were used for uptake studies. Transcellular transport of TMAO was investigated using monolayers of MDCK control cells (MDCK-Co) as well as single- (MDCK-OCT2, MDCK-MATE1) and double-transfected cells (MDCK-OCT2-MATE1). In line with previous studies, HEK-OCT2 cells revealed a 2.4-fold uptake of TMAO compared to control cells (p < 0.001), whereas no significant uptake was observed in HEK-MATE1. In monolayers of MDCK cells, polarised TMAO transcellular transport was not significantly different between MDCK-Co and MDCK-OCT2 cells, but significantly increased in MDCK-MATE1 (p < 0.05) and MDCK-OCT2-MATE1 cells (p < 0.001). The OCT/MATE inhibitor trimethoprim abolished TMAO translocation in MDCK-OCT2-MATE1 cells (p < 0.05). The present data suggest that MATE1 contributes to renal elimination of TMAO. For selected MATE substrates, such as TMAO, uptake studies using non-polarised MATE-expressing cells can reveal false negative results compared to studies using polarised monolayers.
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