ArticleToxins2015
Increased Proinflammatory Cytokine Production and Decreased Cholesterol Efflux Due to Downregulation of ABCG1 in Macrophages Exposed to Indoxyl Sulfate.
Article in Toxins, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 3 of them syntheses that pooled it.
What it found
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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
28 citing papers in PubMed, 3 syntheses or guidelines pooled it, 40 citations in OpenAlex.
- The predictive value of endocan as a novel biomarker: an umbrella study on meta-analyses.Systematic reviews · 2025Pooled it
- Effects of resistant starch supplementation on renal function and inflammatory markers in patients with chronic kidney disease: a meta-analysis of randomized controlled trials.Renal failure · 2024Pooled it
- High circulating endocan in chronic kidney disease? A systematic review and meta-analysis.PloS one · 2023Pooled it
- Trained Immunity as a Mechanistic Bridge Between Uremic Toxins, Atherosclerosis, and Vascular Calcification in Chronic Kidney Disease.Cardiovascular toxicology · 2026Review
- Article
- Valvular calcification in chronic kidney disease: new insights from recent clinical and preclinical studies.Clinical kidney journal · 2025Article
- Vascular inflammation in chronic kidney disease: the role of uremic toxins in macrophage activation.Frontiers in cardiovascular medicine · 2025Review
- Does the Composition of Gut Microbiota Affect Chronic Kidney Disease? Molecular Mechanisms Contributed to Decreasing Glomerular Filtration Rate.International journal of molecular sciences · 2024Review
- Indoxyl Sulfate Contributes to Impaired Height Velocity in (Pre)School Children.Kidney international reports · 2024Article
- Indoxyl Sulfate-Induced Macrophage Toxicity and Therapeutic Strategies in Uremic Atherosclerosis.Toxins · 2024Review
- Uremic Toxins Induce THP-1 Monocyte Endothelial Adhesion and Migration through Specific miRNA Expression.International journal of molecular sciences · 2023Article
- The Contribution of Muscle Innate Immunity to Uremic Cachexia.Nutrients · 2023Review
- Evaluation of Renal Impairment Influence on Metabolic Drug Clearance using a Modelling Approach.Clinical pharmacokinetics · 2023Article
- Indoxyl sulfate induces left ventricular hypertrophyFrontiers in cardiovascular medicine · 2023Article
- Lipid Profile Is Negatively Associated with Uremic Toxins in Patients with Kidney Failure-A Tri-National Cohort.Toxins · 2022Article
- Article
- Review
- Indoxyl-Sulfate-Induced Redox Imbalance in Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2021Review
- Indoxyl Sulfate Mediates the Low Inducibility of the NLRP3 Inflammasome in Hemodialysis Patients.Toxins · 2021Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the possible causes of enhanced atherosclerosis in patients with chronic kidney disease (CKD) is the accumulation of uremic toxins. Since macrophage foam cell formation is a hallmark of atherosclerosis, we examined the direct effect of indoxyl sulfate (IS), a representative uremic toxin, on macrophage function. Macrophages differentiated from THP-1 cells were exposed to IS in vitro. IS decreased the cell viability of THP-1 derived macrophages but promoted the production of inflammatory cytokines (IL-1β, IS 1.0 mM: 101.8 ± 21.8 pg/mL vs. 0 mM: 7.0 ± 0.3 pg/mL, TNF-α, IS 1.0 mM: 96.6 ± 11.0 pg/mL vs. 0 mM: 15.1 ± 3.1 pg/mL) and reactive oxygen species. IS reduced macrophage cholesterol efflux (IS 0.5 mM: 30.3% ± 7.3% vs. 0 mM: 43.5% ± 1.6%) and decreased ATP-binding cassette transporter G1 expression. However, lipid uptake into cells was not enhanced. A liver X receptor (LXR) agonist, T0901317, improved IS-induced production of inflammatory cytokines as well as reduced cholesterol efflux. In conclusion, IS induced inflammatory reactions and reduced cholesterol efflux in macrophages. Both effects of IS were improved with activation of LXR. Direct interactions of uremic toxins with macrophages may be a major cause of atherosclerosis acceleration in patients with CKD.
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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.