ReviewAntioxidants (Basel, Switzerland)2021
Indoxyl-Sulfate-Induced Redox Imbalance in Chronic Kidney Disease.
Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
37 citing papers in PubMed, 59 citations in OpenAlex.
- Molecular Hydrogen and the Uremic Skeleton: A Critical Review and Turnover-State-Dependent Redox Hypothesis in CKD-MBD.Antioxidants (Basel, Switzerland) · 2026Review
- Functional Nanostructured Carbon Honeycomb Monoliths for Hemoadsorption: Preliminary Studies on Biocompatibility, Protein-Bound Uremic Toxins and Inflammatory Cytokines Elimination.International journal of molecular sciences · 2026Article
- Gut Microbiota and Chronic Kidney Disease: A Complex Interplay with Implications for Diagnosis and Treatment.Probiotics and antimicrobial proteins · 2026Review
- Article
- Red Blood Cells in Normal and Pathological States: Redox Reactions of Hemoglobin.Molecules (Basel, Switzerland) · 2026Review
- Assessment of Phenolic and Indolic Compounds Removal from Aqueous Media Using Lignocellulose-Derived Surface-Modified Nanoporous Carbon Adsorbents: A Comparative Study.International journal of molecular sciences · 2026Article
- Altered tryptophan metabolism as a contributor to cognitive impairment in chronic kidney disease: a narrative review.Frontiers in neuroscience · 2026Review
- Plumericin Modulates the AhR-NFκB-Nrf2 Signaling Network to Counteract Indoxyl Sulfate-Induced Intestinal Epithelial Cells Impairment.International journal of molecular sciences · 2025Article
- Plasma metabolomic analysis of patients with different severities acute pancreatitis.World journal of emergency medicine · 2025Article
- Maresin-1 and S-Equol as Emerging Metabolic Biomarkers in Gestational Diabetes-Associated Inflammation.Diagnostics (Basel, Switzerland) · 2025Article
- Protein-energy wasting in chronic kidney disease: mechanisms responsible for loss of muscle mass and function.Kidney research and clinical practice · 2025Article
- Systemic Uremic Toxin Burden in Autism Spectrum Disorder: A Stratified Urinary Metabolite Analysis.International journal of molecular sciences · 2025Article
- Klotho Suppresses Indoxyl Sulfate-Mediated Apoptosis in Human Kidney Proximal Tubular (HK-2) Cells through Modulating the AKT/Nrf2 Mechanism.ACS omega · 2025Article
- Indole metabolism and its role in diabetic macrovascular and microvascular complications.American heart journal plus : cardiology research and practice · 2025Review
- Unveiling the role of sex in the metabolism of indoxyl sulfate and apixaban.Scientific reports · 2025Article
- Gut microbiome dynamics of patients on dialysis: implications for complications and treatment.Frontiers in pharmacology · 2025Review
- Correlation of Indoxyl Sulfate to Hearing Impairment in Chronic Kidney Disease Patients.Iranian journal of otorhinolaryngology · 2025Article
- Association between chronic kidney disease and sarcopenia and emerging treatment strategies.Frontiers in nutrition · 2025Review
- Sulfation pathways in times of change.Essays in biochemistry · 2024Article
- A lipidome landscape of aging in mice.Nature aging · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The accumulation of the uremic toxin indoxyl sulfate (IS) induces target organ damage in chronic kidney disease (CKD) patients, and causes complications including cardiovascular diseases, renal osteodystrophy, muscle wasting, and anemia. IS stimulates reactive oxygen species (ROS) production in CKD, which impairs glomerular filtration by a direct cytotoxic effect on the mesangial cells. IS further reduces antioxidant capacity in renal proximal tubular cells and contributes to tubulointerstitial injury. IS-induced ROS formation triggers the switching of vascular smooth muscular cells to the osteoblastic phenotype, which induces cardiovascular risk. Low-turnover bone disease seen in early CKD relies on the inhibitory effects of IS on osteoblast viability and differentiation, and osteoblastic signaling via the parathyroid hormone. Excessive ROS and inflammatory cytokine releases caused by IS directly inhibit myocyte growth in muscle wasting via myokines' effects. Moreover, IS triggers eryptosis via ROS-mediated oxidative stress, and elevates hepcidin levels in order to prevent iron flux in circulation in renal anemia. Thus, IS-induced oxidative stress underlies the mechanisms in CKD-related complications. This review summarizes the underlying mechanisms of how IS mediates oxidative stress in the pathogenesis of CKD's complications. Furthermore, we also discuss the potential role of oral AST-120 in attenuating IS-mediated oxidative stress after gastrointestinal adsorption of the IS precursor indole.
Indexed as
Identifiers
What OpenQuestion holds
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.