ArticleEndocrinology2012
Chronic inhibition of ERK1/2 signaling improves disordered bone and mineral metabolism in hypophosphatemic (Hyp) mice.
Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 53 citations in OpenAlex.
- The Intricacies of Renal Phosphate Reabsorption-An Overview.International journal of molecular sciences · 2024Review
- Meclozine ameliorates bone mineralization and growth plate structure in a mouse model of X‑linked hypophosphatemia.Experimental and therapeutic medicine · 2023Article
- Interaction of Vitamin D with Peptide Hormones with Emphasis on Parathyroid Hormone, FGF23, and the Renin-Angiotensin-Aldosterone System.Nutrients · 2022Review
- FGF23 and Hypophosphatemic Rickets/Osteomalacia.Current osteoporosis reports · 2021Review
- FGF23 and Vitamin D Metabolism.JBMR plus · 2021Article
- Regulation of bone phosphorus retention and bone development possibly by related hormones and local bone-derived regulators in broiler chicks.Journal of animal science and biotechnology · 2021Article
- Membrane-type 1 Matrix Metalloproteinase Modulates Tissue Homeostasis by a Non-proteolytic Mechanism.iScience · 2020Article
- Osteocytic FGF23 and Its Kidney Function.Frontiers in endocrinology · 2020Review
- FGF23, Hypophosphatemia, and Emerging Treatments.JBMR plus · 2019Review
- Autoimmune hyperphosphatemic tumoral calcinosis in a patient with FGF23 autoantibodies.The Journal of clinical investigation · 2018Article
- Physiological Actions of Fibroblast Growth Factor-23.Frontiers in endocrinology · 2018Review
- Targeting Fibroblast Growth Factor 23 Signaling with Antibodies and Inhibitors, Is There a Rationale?Frontiers in endocrinology · 2018Review
- Pleiotropic Actions of FGF23.Toxicologic pathology · 2017Review
- Therapeutic Effects of FGF23 c-tail Fc in a Murine Preclinical Model of X-Linked Hypophosphatemia Via the Selective Modulation of Phosphate Reabsorption.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2017Article
- X-linked hypophosphatemia and growth.Reviews in endocrine & metabolic disorders · 2017Review
- Effect of Osteocyte-Ablation on Inorganic Phosphate Metabolism: Analysis of Bone-Kidney-Gut Axis.Frontiers in endocrinology · 2017Article
- 1,25-Dihydroxyvitamin D Alone Improves Skeletal Growth, Microarchitecture, and Strength in a Murine Model of XLH, Despite Enhanced FGF23 Expression.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2016Article
- CYP24 inhibition as a therapeutic target in FGF23-mediated renal phosphate wasting disorders.The Journal of clinical investigation · 2016Article
- The PTH-Vitamin D-FGF23 axis.Reviews in endocrine & metabolic disorders · 2015Review
- Characterization of FGF23-Dependent Egr-1 Cistrome in the Mouse Renal Proximal Tubule.PloS one · 2015Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
The X-linked hypophosphatemic (Hyp) mouse carries a loss-of-function mutation in the phex gene and is characterized by hypophosphatemia due to renal phosphate (Pi) wasting, inappropriately suppressed 1,25-dihydroxyvitamin D [1,25(OH)₂D] production, and rachitic bone disease. Increased serum fibroblast growth factor-23 concentration is responsible for the disordered metabolism of Pi and 1,25(OH)₂D. In the present study, we tested the hypothesis that chronic inhibition of fibroblast growth factor-23-induced activation of MAPK signaling in Hyp mice can reverse their metabolic derangements and rachitic bone disease. Hyp mice were administered the MAPK inhibitor, PD0325901 orally for 4 wk. PD0325901 induced a 15-fold and 2-fold increase in renal 1α-hydroxylase mRNA and protein abundance, respectively, and thereby higher serum 1,25(OH)₂D concentrations (115 ± 13 vs. 70 ± 16 pg/ml, P < 0.05), compared with values in vehicle-treated Hyp mice. With PD0325901, serum Pi levels were higher (5.1 ± 0.5 vs. 3 ± 0.2 mg/dl, P < 0.05), and the protein abundance of sodium-dependent phosphate cotransporter Npt2a, was greater than in vehicle-treated mice. The rachitic bone disease in Hyp mice is characterized by abundant unmineralized osteoid bone volume, widened epiphyses, and disorganized growth plates. In PD0325901-treated Hyp mice, mineralization of cortical and trabecular bone increased significantly, accompanied by a decrease in unmineralized osteoid volume and thickness, as determined by histomorphometric analysis. The improvement in mineralization in PD0325901-treated Hyp mice was confirmed by microcomputed tomography analysis, which showed an increase in cortical bone volume and thickness. These findings provide evidence that in Hyp mice, chronic MAPK inhibition improves disordered Pi and 1,25(OH)₂D metabolism and bone mineralization.
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