ArticleToxins2023
Advanced Oxidation Protein Products Contribute to Chronic-Kidney-Disease-Induced Adipose Inflammation through Macrophage Activation.
Article in Toxins, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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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
12 citing papers in PubMed, 11 citations in OpenAlex.
- Albumin as a dynamic extracellular redox regulator: from Cys34 oxidation biomarkers to polysulfide-mediated homeostatic mechanisms and clinical applications.Redox report : communications in free radical research · 2026Review
- The Inflammaging-Redox-InflammamiR Axis in Metabolic Aging: From Diagnostic Clusters to Integrated Risk Phenotypes.Biomolecules · 2026Review
- Therapeutic Regulation of Macrophage Polarization for Diabetic Kidney Disease by Targeted Metabolic Reprogramming.Current medical science · 2026Review
- Targeting perivascular adipose tissue in vascular aging: innovative translational strategies for disease prevention and monitoring.Apoptosis : an international journal on programmed cell death · 2026Review
- White Teff Flour Ethanolic Extract: Phytochemical Profile, Antioxidant and Anti-Inflammatory Activity.Molecules (Basel, Switzerland) · 2026Article
- Chronic Kidney Disease in Patients With Heart Failure With a Preserved Ejection Fraction: The Underlying Role of Visceral Adiposity.Journal of the American College of Cardiology · 2025Review
- Assessment of AOPP, TBARS, and Inflammatory Status in Diabetic Nephropathy and Hemodialyzed Patients.International journal of molecular sciences · 2025Article
- Redox Homeostasis in Red Blood Cells: From Molecular Mechanisms to Antioxidant Strategies.Current issues in molecular biology · 2025Review
- The Clinical Utility and Plausibility of Oxidative and Antioxidant Variables in Chronic and End-Stage Kidney Disease: A Review of the Literature.International journal of molecular sciences · 2025Review
- Evaluation of Xanthine Oxidase Inhibitors Febuxostat and Allopurinol on Kidney Dysfunction and Histological Damage in Two-Kidney, One-Clip (2K1C) Rats.Scientifica · 2025Article
- Nutritional management of pediatric nephrotic syndrome regarding oxidative stress and antioxidant balance.Frontiers in immunology · 2025Review
- Advanced Oxidative Protein Products Had a Diagnostic Accuracy for Identifying Chronic Kidney Disease in Adult Population.Metabolites · 2024Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fat atrophy and adipose tissue inflammation can cause the pathogenesis of metabolic symptoms in chronic kidney disease (CKD). During CKD, the serum levels of advanced oxidation protein products (AOPPs) are elevated. However, the relationship between fat atrophy/adipose tissue inflammation and AOPPs has remained unknown. The purpose of this study was to investigate the involvement of AOPPs, which are known as uremic toxins, in adipose tissue inflammation and to establish the underlying molecular mechanism. In vitro studies involved co-culturing mouse-derived adipocytes (differentiated 3T3-L1) and macrophages (RAW264.7). In vivo studies were performed using adenine-induced CKD mice and AOPP-overloaded mice. Fat atrophy, macrophage infiltration and increased AOPP activity in adipose tissue were identified in adenine-induced CKD mice. AOPPs induced MCP-1 expression in differentiated 3T3-L1 adipocytes via ROS production. However, AOPP-induced ROS production was suppressed by the presence of NADPH oxidase inhibitors and the scavengers of mitochondria-derived ROS. A co-culturing system showed AOPPs induced macrophage migration to adipocytes. AOPPs also up-regulated TNF-α expression by polarizing macrophages to an M1-type polarity, and then induced macrophage-mediated adipose inflammation. In vitro data was supported by experiments using AOPP-overloaded mice. AOPPs contribute to macrophage-mediated adipose inflammation and constitute a potential new therapeutic target for adipose inflammation associated with CKD.
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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.