ArticleJournal of clinical medicine2018
AST-120 Reduces Neuroinflammation Induced by Indoxyl Sulfate in Glial Cells.
Article in Journal of clinical medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 66 citations in OpenAlex.
- Behavioural, neurochemical, and neurohistological effects of bisphenol A and vanadium following chronic co-administration in mice.IBRO neuroscience reports · 2026Article
- From Cognitive Impairment to Uremic Encephalopathy in Chronic Kidney Disease: A Proposed Pathophysiological Continuum.International journal of molecular sciences · 2026Review
- Depression in chronic kidney disease and dialysis: A psychonephrology narrative review.World journal of nephrology · 2026Review
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
- Clinical Pharmacokinetic-Pharmacodynamic Relationships of Pharmacological Strategies for Attenuating p-Cresyl Sulfate in Patients with Kidney Disease.Clinical pharmacokinetics · 2025Article
- Cafeteria and Fast-Food Diets Induce Neuroinflammation, Social Deficits, but a Different Cardiometabolic Phenotype.Nutrients · 2025Article
- Bacterial metabolism of tryptophan causes toxicity inbioRxiv : the preprint server for biology · 2025Article
- Uremic Toxins, CKD, and Cognitive Dysfunction.Journal of the American Society of Nephrology : JASN · 2025Review
- Targeting Inflammatory Imbalance in Chronic Kidney Disease: Focus on Anti-Inflammatory and Resolution Mediators.International journal of molecular sciences · 2025Review
- Protein-bound uremic toxins as therapeutic targets for cardiovascular, kidney, and metabolic disorders.Frontiers in endocrinology · 2025Review
- Regulation of the blood-brain barrier function by peripheral cues in health and disease.Metabolic brain disease · 2024Review
- Indoxyl sulfate induces apoptotic cell death by inhibiting glycolysis in human astrocytes.Kidney research and clinical practice · 2024Article
- AST-120 Protects Cognitive and Emotional Impairment in Chronic Kidney Disease Induced by 5/6 Nephrectomy.Brain sciences · 2024Article
- Increased Blood-Brain Barrier Permeability and Cognitive Impairment in Patients With ESKD.Kidney international reports · 2024Article
- Deficient butyrate metabolism in the intestinal microbiome is a potential risk factor for recurrent kidney stone disease.Urolithiasis · 2024Article
- Gut microbial metabolites SCFAs and chronic kidney disease.Journal of translational medicine · 2024Review
- Irisin Alleviates Cognitive Impairment by Inhibiting AhR/NF-Mediators of inflammation · 2024Article
- Kojic acid reverses LPS-induced neuroinflammation and cognitive impairment by regulating the TLR4/NF-κB signaling pathway.Frontiers in pharmacology · 2024Article
- MiMeDB: the Human Microbial Metabolome Database.Nucleic acids research · 2023Article
- Cellular senescence in brain aging and cognitive decline.Frontiers in aging neuroscience · 2023Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Chronic kidney disease (CKD) involves multiple organ dysfunction, and the neurological complications that are often present in CKD patients support the idea of a crosstalk between the kidneys and the brain. Evidence suggests a possible role for products accumulating in these patients as uremic toxins in various CKD complications, including neurodegeneration. Indoxyl sulfate (IS), derived from tryptophan metabolism, is well-known as a uremic nephron-vascular toxin, and recent evidence suggests it also has a role in the immune response and in neurodegeneration. Inflammation has been associated with neurodegenerative diseases, as well as with CKD. In this study, we demonstrated that sera of CKD patients induced a significant inflammation in astrocyte cells which was proportional to IS sera concentrations, and that the IS adsorbent, AST-120, reduced this inflammatory response. These results indicated that, among the uremic toxins accumulating in serum of CKD patients, IS significantly contributed to astrocyte inflammation. Moreover, being also chronic inflammation associated with CKD, here we reported that IS further increased inflammation and oxidative stress in primary central nervous system (CNS) cells, via Nuclear Factor-κB (NF-κB) and Aryl hydrocarbon Receptor (AhR) activation, and induced neuron death. This study is a step towards elucidating IS as a potential pharmacological target in CKD patients.
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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.