ReviewExperimental physiology2025
Molecular pathophysiology of chronic kidney disease-mineral and bone disorder: Focus on the fibroblast growth factor 23-Klotho axis and bone turnover dynamics.
Review in Experimental physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed.
- Biomaterials at the interface of bone-derived factors and inter-organ communication: Current evidence and future perspectives.Bioactive materials · 2026Review
- Temporomandibular Joint Abnormalities in Hemodialysis Patients: A Cross-Sectional Ultrasonographic Study from a Single Center in Italy.Medical sciences (Basel, Switzerland) · 2026Article
- Calcidiol Status and Metabolic Syndrome in 40-60-Year-Old Women: Association with Metabolic Components.Nutrients · 2026Article
- Pre-Parathyroidectomy PTH as an Integrated Biomarker of Glandular Remodeling and Skeletal Turnover in Secondary Hyperparathyroidism.International journal of molecular sciences · 2026Review
- Article
- Organokine-Mediated Crosstalk: A Systems Biology Perspective on the Pathogenesis of MASLD-A Narrative Review.International journal of molecular sciences · 2025Review
- Molecular pathophysiology of chronic kidney disease-mineral and bone disorder: Focus on the fibroblast growth factor 23-Klotho axis and bone turnover dynamics.Experimental physiology · 2025Review
- Serum creatinine, genetic susceptibility, and the risk of osteoporosis and fracture: a prospective cohort study from the UK Biobank.Frontiers in endocrinology · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a major complication of chronic kidney disease (CKD), characterized by disruptions in mineral metabolism, abnormal bone turnover and vascular calcification, which collectively increase the risk of fractures and cardiovascular disease. This review examines the molecular mechanisms underlying CKD-MBD, with a particular focus on the fibroblast growth factor 23 (FGF23)-Klotho axis - a key regulator of phosphate balance, vitamin D activation and parathyroid hormone secretion. In CKD, elevated FGF23 levels and reduced Klotho expression contribute to mineral homeostasis disturbances and bone abnormalities. The dysregulation of this pathway plays a central role in CKD-MBD pathophysiology and its associated complications. Emerging therapies, such as anti-FGF23 antibodies and recombinant Klotho, hold promise for modulating FGF23 activity and restoring mineral balance. This review highlights the importance of individualized treatment strategies based on bone turnover patterns and FGF23-Klotho axis dysfunction. Advancing our understanding of these molecular mechanisms will aid in the development of more effective diagnostic tools and therapeutic interventions to improve CKD-MBD outcomes.
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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.