ArticleJournal of applied toxicology : JAT2022
Effects of the uremic toxin indoxyl sulphate on human microvascular endothelial cells.
Article in Journal of applied toxicology : JAT, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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.
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- Can the Posterior Segment Findings of the Eye and Serum Microbiota Metabolites Be a Biomarker in Schizophrenia?Medicina (Kaunas, Lithuania) · 2026Article
- Gene expression kinetics in Sepsis After Cardiac Surgery (SACS): a multicentric prospective observational study.Journal of anesthesia, analgesia and critical care · 2025Article
- Review
- Article
- Irisin Alleviates Cognitive Impairment by Inhibiting AhR/NF-Mediators of inflammation · 2024Article
- Indoxyl sulfate induces apoptosis in mononuclear blood cells via mitochondrial pathway.Scientific reports · 2023Article
- Zebrafish as a Model of Cardiac Pathology and Toxicity: Spotlight on Uremic Toxins.International journal of molecular sciences · 2023Review
- Gut-Derived Uremic Toxins in CKD: An Improved Approach for the Evaluation of Serum Indoxyl Sulfate in Clinical Practice.International journal of molecular sciences · 2023Article
- Effects of the uremic toxin indoxyl sulphate on human microvascular endothelial cells.Journal of applied toxicology : JAT · 2022Article
- Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Indoxyl sulphate (IS) is a uremic toxin accumulating in the plasma of chronic kidney disease (CKD) patients. IS accumulation induces side effects in the kidneys, bones and cardiovascular system. Most studies assessed IS effects on cell lines by testing higher concentrations than those measured in CKD patients. Differently, we exposed a human microvascular endothelial cell line (HMEC-1) to the IS concentrations measured in the plasma of healthy subjects (physiological) or CKD patients (pathological). Pathological concentrations reduced cell proliferation rate but did not increase long-term oxidative stress level. Indeed, total protein thiols decreased only after 24 h of exposure in parallel with an increased Nrf-2 protein expression. IS induced actin cytoskeleton rearrangement with formation of stress fibres. Proteomic analysis supported this hypothesis as many deregulated proteins are related to actin filaments organization or involved in the endothelial to mesenchymal transition. Interestingly, two proteins directly linked to cardiovascular diseases (CVD) in in vitro and in vivo studies underwent deregulation: COP9 signalosome complex subunit 9 and thrombomodulin. Future experiments will be needed to investigate the role of these proteins and the signalling pathways in which they are involved to clarify the possible link between CKD and CVD.
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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 Socratic graph.