Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

FGF23 suppresses chondrocyte proliferation in the presence of soluble α-Klotho both in vitro and in vivo.

The Journal of biological chemistry - 25 Jan 2013

Kawai Masanobu, Kinoshita Saori, Kimoto Akihito, Hasegawa Yasuhiro, Miyagawa Kazuaki, Yamazaki Miwa, Ohata Yasuhisa, Ozono Keiichi, Michigami Toshimi

Abstract excerpt

Fibroblast growth factor-23 (FGF23) is well established to play crucial roles in the regulation of phosphate homeostasis. X-linked hypophosphatemic rickets (XLH) is characterized by impaired mineralization and growth retardation associated with elevated circulating FGF23 levels. Administration of phosphate and calcitriol is effective in improving growth retardation, but is not sufficient to fully reverse impaired...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Chondrocytes
Share to Chondrogenesis

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Familial Hypophosphatemic Rickets

Share to Fibroblast Growth Factor-23

Share to Fibroblast Growth Factors

Share to Genetic Diseases, X-Linked

Share to Glucuronidase

Share to Klotho Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 23235154
DOI: 10.1074/jbc.M112.410043
PMCID: PMC3554911

Genes

FGF23
FGFR3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

FGF23 suppresses chondrocyte proliferation in the presence of soluble α-Klotho both in vitro and in vivo.PMID 23235154Read ↗

X-Linked Hypophosphatemia: A Review of Pathophysiology, Clinical Manifestations, Current Management, and Emerging Therapeutic StrategiesSemantic proximity Read ↗

FGF23–GH Crosstalk in Phosphate Allocation and Growth Plate BiologySemantic proximity Read ↗

Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient mice.Semantic proximity Read ↗

FGF23 and its role in X-linked hypophosphatemia-related morbiditySemantic proximity Read ↗

The FGF23/KLOTHO Regulatory Network and Its Roles in Human Disorders.Semantic proximity Read ↗

FGF23 in skeletal modeling and remodeling.Semantic proximity Read ↗

Circulating αKlotho influences phosphate handling by controlling FGF23 production.Semantic proximity Read ↗

In vivo genetic evidence for klotho-dependent, fibroblast growth factor 23 (Fgf23) -mediated regulation of systemic phosphate homeostasis.Semantic proximity Read ↗

X-linked hypophosphatemic rickets and craniosynostosis.Semantic proximity Read ↗

Mineralizing enthesopathy is a common feature of renal phosphate-wasting disorders attributed to FGF23 and is exacerbated by standard therapy in hyp mice.Semantic proximity Read ↗

Survey of the enthesopathy of X-linked hypophosphatemia and its characterization in Hyp mice.Semantic proximity Read ↗

Nuclear isoforms of fibroblast growth factor 2 are novel inducers of hypophosphatemia via modulation of FGF23 and KLOTHO.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.