ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2011
FGF-23/Klotho signaling is not essential for the phosphaturic and anabolic functions of PTH.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- The rationale for intermittent administration of PTH in the management of mineral and bone disorder of chronic kidney disease.Journal of nephrology · 2024Review
- Progress of Wnt Signaling Pathway in Osteoporosis.Biomolecules · 2023Review
- Use of Teriparatide in Hyperphosphatemic Familial Tumor Calcinosis: Evaluating the Interaction Between FGF23 and PTH on the Phosphaturic Effect.Calcified tissue international · 2022Article
- Pathophysiology of Vascular Calcification and Bone Loss: Linked Disorders of Ageing?Nutrients · 2021Review
- Anabolic actions of PTH in murine models: two decades of insights.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- Phosphate and fibroblast growth factor 23 in diabetes.Clinical science (London, England : 1979) · 2021Review
- Understanding the Stony Bridge between Osteoporosis and Vascular Calcification: Impact of the FGF23/Klotho axis.Oxidative medicine and cellular longevity · 2021Review
- The Klotho proteins in health and disease.Nature reviews. Nephrology · 2019Review
- Mettl3-mediated mNature communications · 2018Article
- Guanylate Binding Protein 1 Inhibits Osteogenic Differentiation of Human Mesenchymal Stromal Cells Derived from Bone Marrow.Scientific reports · 2018Article
- Bone quality changes associated with aging and disease: a review.Annals of the New York Academy of Sciences · 2017Review
- Fructus Ligustri Lucidi in Osteoporosis: A Review of its Pharmacology, Phytochemistry, Pharmacokinetics and Safety.Molecules (Basel, Switzerland) · 2017Review
- The Association Between Fibroblast Growth Factor 23 and Renal Transplantation Outcome Is Modified by Follow-up Duration and Glomerular Filtration Rate Assessment Method.Kidney international reports · 2017Article
- Review
- Acute Parathyroid Hormone Injection Increases C-Terminal but Not Intact Fibroblast Growth Factor 23 Levels.Endocrinology · 2017Article
- FGF23 Is Not Required to Regulate Fetal Phosphorus Metabolism but Exerts Effects Within 12 Hours After Birth.Endocrinology · 2017Article
- Parathyroid hormone 1 receptor is essential to induce FGF23 production and maintain systemic mineral ion homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Fibroblast Growth Factor Receptor 3 Deficiency Does Not Impair the Osteoanabolic Action of Parathyroid Hormone on Mice.International journal of biological sciences · 2016Article
- DNA NBone research · 2016Article
- Fibroblast growth factor 23 and bone mineralisation.International journal of oral science · 2015Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Parathyroid hormone (PTH) is widely recognized as a key regulator of mineral ion homeostasis. Daily intermittent administration of PTH is the only currently available anabolic therapy for bone disorders such as osteoporosis. Recent studies have shown that PTH increases transcription and secretion of fibroblast growth factor 23 (FGF-23), another important regulator of phosphate homeostasis and skeletal metabolism. However, the full relationship between PTH and FGF-23 is largely unknown. This study evaluated the effect of FGF-23/Klotho signaling on the phosphaturic and anabolic functions of PTH. Eight-day-old wild-type (WT) Fgf23(-/-) and Kl(-/-) mice were injected with 100 µg/kg PTH(1-34) or vehicle daily for a 2-week-period and then euthanized. Intermittent injection of PTH successfully reduced the serum phosphate levels and reversed the hyperphosphatemia of Fgf23(-/-) and Kl(-/-) mice. Bone changes were analyzed in the distal femur metaphysis by peripheral quantitative computed tomography (pQCT), micro-computed tomography (µCT), and histomorphometry. PTH treatment induced substantial increases in bone mineral density (BMD) and trabecular bone volume in each mouse genotype. Expression of osteoblastic marker genes, including Runx2, Col1, Alp, Ocn, and Sost, was similarly altered. In addition, primary osteoblasts were isolated and treated with 100 nM PTH in vitro. PTH treatment similarly induced cAMP accumulation and phosphorylation of ERK1/2 and CREB in the osteoblasts from each genotype. Taken together, our results demonstrate that FGF-23/Klotho signaling is not essential for the phosphaturic and anabolic functions of PTH, suggesting that PTH can function as a therapeutic agent to improve the skeletal quality of patients even in the presence of abnormal serum FGF-23 levels.
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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.