ArticleInternational journal of molecular sciences2019
Effect of Indoxyl Sulfate on the Repair and Intactness of Intestinal Epithelial Cells: Role of Reactive Oxygen Species' Release.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 54 citations in OpenAlex.
- Article
- Plumericin Modulates the AhR-NFκB-Nrf2 Signaling Network to Counteract Indoxyl Sulfate-Induced Intestinal Epithelial Cells Impairment.International journal of molecular sciences · 2025Article
- Review
- Targeting Inflammatory Imbalance in Chronic Kidney Disease: Focus on Anti-Inflammatory and Resolution Mediators.International journal of molecular sciences · 2025Review
- Gut microbiota regulates oxidative stress and inflammation: a double-edged sword in renal fibrosis.Cellular and molecular life sciences : CMLS · 2024Review
- Brain-Gut and Microbiota-Gut-Brain Communication in Type-2 Diabetes Linked Alzheimer's Disease.Nutrients · 2024Review
- Gut microbiota and functional dyspepsia: a two-sample Mendelian randomization study.Frontiers in microbiology · 2024Article
- An Overview of Chronic Kidney Disease Pathophysiology: The Impact of Gut Dysbiosis and Oral Disease.Biomedicines · 2023Review
- Indoxyl sulfate induces apoptosis in mononuclear blood cells via mitochondrial pathway.Scientific reports · 2023Article
- Review
- Cyclic GMP-AMP Synthase (cGAS) Deletion Reduces Severity in Bilateral Nephrectomy Mice through Changes in Neutrophil Extracellular Traps and Mitochondrial Respiration.Biomedicines · 2023Article
- Exploration of the anti-hyperuricemia effect of TongFengTangSan (TFTS) by UPLC-Q-TOF/MS-based non-targeted metabonomics.Chinese medicine · 2023Article
- Article
- TrimethylamineNutrients · 2022Article
- Indoxyl Sulfate Induces Oxidative Changes in Plasma and Hemolysate.Molecules (Basel, Switzerland) · 2022Article
- Short-Chain Fatty Acids in Chronic Kidney Disease: Focus on Inflammation and Oxidative Stress Regulation.International journal of molecular sciences · 2022Review
- Production of Indole and Indole-Related Compounds by the Intestinal Microbiota and Consequences for the Host: The Good, the Bad, and the Ugly.Microorganisms · 2022Review
- What If Not All Metabolites from the Uremic Toxin Generating Pathways Are Toxic? A Hypothesis.Toxins · 2022Review
- Dual Role of Indoles Derived From Intestinal Microbiota on Human Health.Frontiers in immunology · 2022Review
- Abdominal massage alleviates functional diarrhea in immature rats via modulation of intestinal microbiota and tight junction protein.Frontiers in pediatrics · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Chronic kidney disease (CKD) is characterized by an oxidative stress status, driving some CKD-associated complications, even at the gastrointestinal level. Indoxyl Sulfate (IS) is a protein-bound uremic toxin, poorly eliminated by dialysis. This toxin is able to affect the intestinal system, but its molecular mechanism/s in intestinal epithelial cells (IECs) remain poorly understood. This study's aim was to evaluate the effect of IS (31.2-250 µM) on oxidative stress in IEC-6 cells and on the intactness of IECs monolayers. Our results indicated that IS enhanced oxidative cell damage by inducing reactive oxygen species (ROS) release, reducing the antioxidant response and affecting Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) nuclear translocation as well its related antioxidant enzymes. In the wound healing assay model, IS reduced IEC-6 migration, slightly impaired actin cytoskeleton rearrangement; this effect was associated with connexin 43 alteration. Moreover, we reported the effect of CKD patients' sera in IEC-6 cells. Our results indicated that patient sera induced ROS release in IEC-6 cells directly related to IS sera content and this effect was reduced by AST-120 serum treatment. Results highlighted the effect of IS in inducing oxidative stress in IECs and in impairing the intactness of the IECs cell monolayer, thus significantly contributing to CKD-associated intestinal alterations.
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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.