ArticleFrontiers in pharmacology2017
Indoxyl Sulfate Affects Glial Function Increasing Oxidative Stress and Neuroinflammation in Chronic Kidney Disease: Interaction between Astrocytes and Microglia.
Article in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 3 of them syntheses that pooled it.
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Who cites it
128 citing papers in PubMed, 3 syntheses or guidelines pooled it, 166 citations in OpenAlex.
- Indoxyl Sulfate and Autism Spectrum Disorder: A Literature Review.International journal of molecular sciences · 2024Pooled it
- Specific alterations of gut microbiota in patients with membranous nephropathy: A systematic review and meta-analysis.Frontiers in physiology · 2022Pooled it
- Pooled it
- From Cognitive Impairment to Uremic Encephalopathy in Chronic Kidney Disease: A Proposed Pathophysiological Continuum.International journal of molecular sciences · 2026Review
- Chronic kidney disease and cognitive decline: choroid plexus remodeling, glymphatic dysfunction, and alzheimer biomarker interpretation.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Review
- Rewiring of NestinNeuroscience bulletin · 2026Article
- AKI as a systemic syndrome and its impact on other organ systems.Critical care (London, England) · 2026Review
- Article
- Neuro-Renal Crosstalk Across the Chronic Kidney Disease Spectrum: Stage-Dependent Molecular Mechanisms of Cognitive Impairment-An Integrative Review.International journal of molecular sciences · 2026Review
- Targeting Uremic Toxins in Chronic Kidney Disease: Current Challenges and Emerging Therapeutic Strategies.Toxins · 2026Review
- The Kidney-Brain Axis in Chronic Kidney Disease: Uremic Toxins, Cognitive Decline, Mechanistic Pathways, Biomarkers and Therapeutic Perspectives.Biomedicines · 2026Review
- Select microbial metabolites promote tau aggregation in a murine tauopathy model.Nature communications · 2026Article
- Simultaneous quantification of total and free protein-bound uremic toxins in serum by LC-MS/MS: method development, validation, and clinical application in hemodialysis patients.BMC chemistry · 2026Article
- From Parallel Programming to Bidirectional Crosstalk: The Brain-Kidney Axis in Cardiovascular-Kidney-Metabolic Syndrome.Antioxidants (Basel, Switzerland) · 2026Review
- Mind the Gut: Cognitive Decline, Microbiota, and Nutrition-Related Modulators in Older Adults with Chronic Kidney Disease.Nutrients · 2026Review
- Interconnected influences of diet, gut microbiome, and metabolome on cognition across three metabolomics platforms.Research square · 2026Article
- Microglial Ccl4-Ccr5 signaling links systemic inflammation to synaptic loss and memory deficits in chronic kidney disease.Journal of neuroinflammation · 2026Article
- Associations Between Renal Function, Uremic Toxins, and Cognitive Performance in Patients with Chronic Kidney Disease: A Pilot Study.International journal of medical sciences · 2026Observational
- A machine learning model integrating gut microbiota biomarkers for predicting neurological recovery after cerebral hypoxia-ischemia: a single-center study augmented with public data.Frontiers in pharmacology · 2026Article
- Combined Maternal and Offspring Vitamin D3 Supplementation Ameliorates Autism-Like Behaviors via VDR Pathway Activation, Neuroinflammatory Suppression, and Metabolic Homeostasis Restoration.International journal of general medicine · 2026Article
68 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Indoxyl sulfate (IS) is a protein-bound uremic toxin resulting from the metabolism of dietary tryptophan which accumulates in patients with impaired renal function, such as chronic kidney disease (CKD). IS is a well-known nephrovascular toxin but little is known about its effects on central nervous system (CNS) cells. Considering the growing interest in the field of CNS comorbidities in CKD, we studied the effect of IS on CNS cells. IS (15-60 μM) treatment in C6 astrocyte cells increased reactive oxygen species release and decreased nuclear factor (erythroid-derived 2)-like 2 (Nrf2) activation, and heme oxygenase-1 (HO-1) and NAD(P)H dehydrogenase quinone 1 expression. Moreover, IS increased Aryl hydrocarbon Receptor (AhR) and Nuclear Factor-kB (NF-kB) activation in these cells. Similiar observations were made in primary mouse astrocytes and mixed glial cells. Inducible nitric oxide synthase and cyclooxygenase-2 (COX-2) expression, tumor necrosis factor-α and interleukin-6 release and nitrotyrosine formation were increased by IS (15-60 μM) in primary mouse astrocytes and mixed glial cells. IS increased AhR and NF-kB nuclear translocation and reduced Nrf2 translocation and HO-1 expression in primary glial cells. In addition, IS induced cell death in neurons in a dose dependent fashion. Injection of IS (800 mg/kg, i.p.) into mice induced histological changes and increased COX-2 expression and nitrotyrosine formation in thebrain tissue. Taken together, our results show a significant contribution of IS in generating a neurotoxic enviroment and it could also have a potential role in neurodegeneration. IS could be considered also a potential therapeutical target for CKD-associated neurodegenerative complications.
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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.