ArticleJournal of ophthalmology2023
Trimethylamine-N-Oxide Promotes High-Glucose-Induced Dysfunction and NLRP3 Inflammasome Activation in Retinal Microvascular Endothelial Cells.
Article in Journal of ophthalmology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- The microbiome-derived metabolite trimethylamine N-oxide is associated with chronic kidney disease risk.Applied microbiology and biotechnology · 2025Pooled it
- Marine-Derived Proteins: Individual Variability in Health Effects Across Protein Structure, Host Genetics, and Gut Microbiota.Comprehensive reviews in food science and food safety · 2026Review
- The gut-retina axis in diabetic retinopathy: a new paradigm for pathogenesis and therapeutic intervention.Frontiers in immunology · 2026Review
- PTIP inhibits proliferation, migration, and angiogenesis of retinal microvascular endothelial cells in a high-glucose environment.In vitro cellular & developmental biology. Animal · 2026Article
- The gut-eye axis in blinding eye diseases: microbiota-driven immune dysregulation and immunomodulatory therapies.International ophthalmology · 2025Review
- Targeting the gut-retina axis: mechanistic insights and therapeutic prospects for diabetic retinopathy.Inflammopharmacology · 2025Review
- TMAO and diabetes: from the gut feeling to the heart of the problem.Nutrition & diabetes · 2025Review
- The role of gut microbiota dysbiosis in the inflammatory pathogenesis of diabetic retinopathy.Frontiers in immunology · 2025Review
- Global trends and hotspots of inflammation in diabetic retinopathy: a literature review and bibliometric analysis.Frontiers in medicine · 2025Review
- Postbiotics: emerging therapeutic approach in diabetic retinopathy.Frontiers in microbiology · 2024Review
- Trimethylamine N-Oxide (TMAO) Inducing Endothelial Injury: UPLC-MS/MS-Based Quantification and the Activation of Cathepsin B-Mediated NLRP3 Inflammasome.Molecules (Basel, Switzerland) · 2023Article
- The gut-retina axis: a new perspective in the prevention and treatment of diabetic retinopathy.Frontiers in endocrinology · 2023Review
- Research progress of diabetic retinopathy and gut microecology.Frontiers in microbiology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Along with blood glucose levels, diabetic retinopathy (DR) development also involves endogenous risk factors, such as trimethylamine-N-oxide (TMAO), a product of intestinal flora metabolic disorder, which exacerbates diabetic microvascular complications. However, the effect of TMAO on retinal cells under high-glucose conditions remains unclear. Therefore, this study examined the effects of TMAO on high-glucose-induced retinal dysfunction in the context of NLRP3 inflammasome activation, which is involved in DR. Materials and Methods: TMAO was assessed in the serum and aqueous humor of patients using ELISA. Human retinal microvascular endothelial cells (HRMECs) were treated for 72 h as follows: NG (normal glucose, D-glucose 5.5 mM), NG + TMAO (5 Results: The serum and aqueous humor from patients with PDR contained higher levels of TMAO compared to patients with nontype 2 diabetes (Control), non-DR (NDR), and non-PDR (NPDR). TMAO showed significant acceleration of high-glucose-induced cell proliferation, wound healing, cell migration, and tube formation. ZO-1 expression decreased remarkably with the combined action of TMAO and a high glucose compared to either treatment alone. TMAO also promoted high-glucose-activated NLRP3 inflammasome complex. Conclusion: The combination of TMAO and high-glucose results in increased levels of ROS and NLRP3 inflammasome complex activation in HRMECs, leading to exacerbated retinal dysfunction and barrier failure. Thus, TMAO can accelerate PDR occurrence and development, thus indicating the need for early fundus monitoring in diabetic patients with intestinal flora disorders.
Identifiers
What OpenQuestion holds
Registered trials
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.