ArticleeLife2022
Hyperphosphatemia increases inflammation to exacerbate anemia and skeletal muscle wasting independently of FGF23-FGFR4 signaling.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- The effect of high-dose vitamin D supplementation on hepcidin-25 and erythropoiesis in patients with chronic kidney disease.BMC nephrology · 2023Trial
- Inorganic phosphate: a link between processed food and exercise intolerance in the modern world.Clinical science (London, England : 1979) · 2026Review
- Review
- Myostatin Research: From Molecular Understanding to Clinical Translation for Musculoskeletal and Metabolic Disorders.International journal of molecular sciences · 2026Review
- Macrophage ferritin heavy chain/α-synuclein regulatory axis modulates ferroptosis during kidney injury.JCI insight · 2026Article
- Association between admission serum phosphate levels and prognosis in post-cardiac arrest patients: a retrospective observational study.BMC cardiovascular disorders · 2026Observational
- The effects of elevated phosphate on the kidney - damaging the gatekeeper.Pflugers Archiv : European journal of physiology · 2026Review
- The renal response to FGF23 shifts from phosphaturia toward inflammation in kidney disease.Journal of cell communication and signaling · 2026Article
- Nutritional and Metabolic Interventions to Prevent and Treat Protein-Energy Wasting in Nondialysis CKD-Narrative Review.Nutrients · 2026Review
- The Pathogenic Roles of Local Vitamin D Metabolism Defect in Valve Inflammation and Calcification.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Multiscale Analysis Reveals Altered Characteristics in Femur and Mandible of Mice on a High Phosphate Diet.Calcified tissue international · 2025Article
- Soft tissue calcifications in chronic kidney disease-beyond the vasculature.Pflugers Archiv : European journal of physiology · 2025Review
- Disease-modifying effects of iron deficiency in mouse models of chronic renal failure.Blood red cells & iron · 2025Article
- The Pathologic Actions of Phosphate in CKD.Kidney360 · 2025Review
- Uric Acid Correlates with Serum Levels of Mineral Bone Metabolism and Inflammation Biomarkers in Patients with Stage 3a-5 Chronic Kidney Disease.Medicina (Kaunas, Lithuania) · 2024Article
- Chronic Kidney Disease-associated Lung Injury Is Mediated by Phosphate-induced MAPK/AKT Signaling.American journal of respiratory cell and molecular biology · 2024Article
- Hyperphosphatemia Contributes to Skeletal Muscle Atrophy in Mice.International journal of molecular sciences · 2024Article
- The role of osteopontin and osteocyte-derived factors in secondary hyperparathyroidism-induced myopathy.JBMR plus · 2024Article
- Skeletal Muscle Injury in Chronic Kidney Disease-From Histologic Changes to Molecular Mechanisms and to Novel Therapies.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Elevations in plasma phosphate concentrations (hyperphosphatemia) occur in chronic kidney disease (CKD), in certain genetic disorders, and following the intake of a phosphate-rich diet. Whether hyperphosphatemia and/or associated changes in metabolic regulators, including elevations of fibroblast growth factor 23 (FGF23) directly contribute to specific complications of CKD is uncertain. Here, we report that similar to patients with CKD, mice with adenine-induced CKD develop inflammation, anemia, and skeletal muscle wasting. These complications are also observed in mice fed high phosphate diet even without CKD. Ablation of pathologic FGF23-FGFR4 signaling did not protect mice on an increased phosphate diet or mice with adenine-induced CKD from these sequelae. However, low phosphate diet ameliorated anemia and skeletal muscle wasting in a genetic mouse model of CKD. Our mechanistic in vitro studies indicate that phosphate elevations induce inflammatory signaling and increase hepcidin expression in hepatocytes, a potential causative link between hyperphosphatemia, anemia, and skeletal muscle dysfunction. Our study suggests that high phosphate intake, as caused by the consumption of processed food, may have harmful effects irrespective of pre-existing kidney injury, supporting not only the clinical utility of treating hyperphosphatemia in CKD patients but also arguing for limiting phosphate intake in healthy individuals.
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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.