ArticleInflammation2016
Trimethylamine-N-Oxide Treatment Induces Changes in the ATP-Binding Cassette Transporter A1 and Scavenger Receptor A1 in Murine Macrophage J774A.1 cells.
Article in Inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 53 citations in OpenAlex.
- Review
- 3-Hydroxystearic acid promotes cholesterol efflux and attenuates atherosclerosis via the ALKBH5/PAX-8/ABCA1 pathway.Frontiers in immunology · 2026Article
- Gut microbiota-cholesterol crosstalk in cardiovascular diseases: mechanisms, metabolites, and therapeutic modulation.Nutrition & metabolism · 2025Review
- Gut microbiota: a novel strategy affecting atherosclerosis.Microbiology spectrum · 2025Review
- Gut Microbe-Generated Metabolite Trimethylamine-N-Oxide and Ischemic Stroke.Biomolecules · 2024Review
- Role of Gut Microbial Metabolites in Cardiovascular Diseases-Current Insights and the Road Ahead.International journal of molecular sciences · 2024Review
- The Gut Microbiome Affects Atherosclerosis by Regulating Reverse Cholesterol Transport.Journal of cardiovascular translational research · 2024Review
- Gut microbiota-host lipid crosstalk in Alzheimer's disease: implications for disease progression and therapeutics.Molecular neurodegeneration · 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
- A Blood-based Metabolite Signature for Personalized Risk Assessment of Pancreatic Cancer.Journal of cancer immunology · 2024Article
- Trimethylamine N-Oxide as a Mediator Linking Peripheral to Central Inflammation: An In Vitro Study.International journal of molecular sciences · 2023Article
- The roles of trimethylamine-N-oxide in atherosclerosis and its potential therapeutic aspect: A literature review.Biomolecules & biomedicine · 2023Review
- Gut Molecules in Cardiometabolic Diseases: The Mechanisms behind the Story.International journal of molecular sciences · 2023Review
- Microbiota Effect on Trimethylamine N-Oxide Production: From Cancer to Fitness-A Practical Preventing Recommendation and Therapies.Nutrients · 2023Review
- Gut Microbiota-Derived TMAO: A Causal Factor Promoting Atherosclerotic Cardiovascular Disease?International journal of molecular sciences · 2023Review
- Mitochondria as novel mediators linking gut microbiota to atherosclerosis that is ameliorated by herbal medicine: A review.Frontiers in pharmacology · 2023Review
- Targeting gut microbiota and immune crosstalk: potential mechanisms of natural products in the treatment of atherosclerosis.Frontiers in pharmacology · 2023Review
- The role of the gut microbiota in health and cardiovascular diseases.Molecular biomedicine · 2022Review
- The associations between TMAO-related metabolites and blood lipids and the potential impact of rosuvastatin therapy.Lipids in health and disease · 2022Article
- Trimethylamine N-oxide and its precursors in relation to blood pressure: A mendelian randomization study.Frontiers in cardiovascular medicine · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecently, trimethylamine N-oxide was introduced as a risk factor for atherosclerosis in terms of helping foam cell formation and worsening atherosclerosis complications. The present study was performed to investigate whether/how trimethylamine N-oxide is involved in regulation of ATP-binding cassette transporter A1 and scavenger receptor A1 in macrophages at both mRNA and protein levels.
methodsMurine macrophage J774A.1 cells were treated with micromolar concentrations of trimethylamine N-oxide and 4-phenylbutyric acid, a chemical chaperon, for different time intervals. Tunicamycin was also used as a control for induction of endoplasmic reticulum stress.
resultsSimilar to tunicamycin, trimethylamine N-oxide increased scavenger receptor A1 in all treatment periods, whereas ATP-binding cassette transporter A1 was only reduced 24 h post-treatment with trimethylamine N-oxide at both mRNA and protein levels. In contrast, 4-phenylbutyric acid failed to induce such changes in either scavenger receptor A1 or ATP-binding cassette transporter A1.
conclusionsThe results of this study, in agreement with previous studies, confirm the mechanistic role of trimethylamine N-oxide in the upregulation of scavenger receptor A1, which potentially can promote its proatherogenic role. The results also showed downregulation of ATP-binding cassette transporter A1 in trimethylamine N-oxide treated macrophages which may indicate another possible proatherosclerotic mechanism for foam cell formation.
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