ArticleFrontiers in endocrinology2018
Augmented Fibroblast Growth Factor-23 Secretion in Bone Locally Contributes to Impaired Bone Mineralization in Chronic Kidney Disease in Mice.
Article in Frontiers in endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 24 citations in OpenAlex.
- Impaired bone matrix maturation and mineralization are prevalent in adolescent end-stage kidney disease.JBMR plus · 2026Article
- Fibroblast growth factor 23: Regulation, signalling and systemic links between bone, metabolism and inflammation.Molecular metabolism · 2026Review
- Advances in noninvasive diagnosis of renal osteodystrophy.Renal failure · 2025Review
- Development of animal models with chronic kidney disease-mineral and bone disorder based on clinical characteristics and pathogenesis.Frontiers in endocrinology · 2025Review
- Non-Classical Effects of FGF23: Molecular and Clinical Features.International journal of molecular sciences · 2024Review
- Mouse Models of Mineral Bone Disorders Associated with Chronic Kidney Disease.International journal of molecular sciences · 2023Review
- Fibroblast Growth Factor 23 and Osteoporosis: Evidence from Bench to Bedside.International journal of molecular sciences · 2022Review
- Renal failure suppresses muscle irisin expression, and irisin blunts cortical bone loss in mice.Journal of cachexia, sarcopenia and muscle · 2022Article
- Article
- New Insights to the Crosstalk between Vascular and Bone Tissue in Chronic Kidney Disease-Mineral and Bone Disorder.Metabolites · 2021Review
- How FGF23 shapes multiple organs in chronic kidney disease.Molecular and cellular pediatrics · 2021Review
- A phosphate and calcium-enriched diet promotes progression of 5/6-nephrectomy-induced chronic kidney disease in C57BL/6 mice.Scientific reports · 2021Article
- Aldosterone Is Positively Associated With Circulating FGF23 Levels in Chronic Kidney Disease Across Four Species, and May Drive FGF23 Secretion Directly.Frontiers in physiology · 2021Article
- Hypoxia Pathway Proteins are Master Regulators of Erythropoiesis.International journal of molecular sciences · 2020Review
- Increased FGF-23 levels are linked to ineffective erythropoiesis and impaired bone mineralization in myelodysplastic syndromes.JCI insight · 2020Article
- Transcriptomics: a Solution for Renal Osteodystrophy?Current osteoporosis reports · 2020Review
- The EPO-FGF23 Signaling Pathway in Erythroid Progenitor Cells: Opening a New Area of Research.Frontiers in physiology · 2019Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a systemic disorder of mineral and bone metabolism caused by CKD. Impaired bone mineralization together with increased bony secretion of fibroblast growth factor-23 (FGF23) are hallmarks of CKD-MBD. We recently showed that FGF23 suppresses the expression of tissue nonspecific alkaline phosphatase (TNAP) in bone cells by a Klotho-independent, FGF receptor-3-mediated signaling axis, leading to the accumulation of the mineralization inhibitor pyrophosphate. Therefore, we hypothesized that excessive FGF23 secretion may locally impair bone mineralization in CKD-MBD. To test this hypothesis, we induced CKD by 5/6 nephrectomy in 3-month-old wild-type (WT) mice and
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Registered trials
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