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Article

Hypophosphatemia-mediated hypotension in transgenic mice overexpressing human FGF-23.

American journal of physiology. Heart and circulatory physiology - 1 Oct 2009

Liu Peidang, Bai Xiuying, Wang Heming, Karaplis Andrew, Goltzman David, Miao Dengshun

Abstract excerpt

Fibroblast growth factor-23 (FGF-23) is a potent circulating phosphaturic factor associated with renal phosphate wasting. The effects of FGF-23 on skeletal and phosphate homeostasis have been investigated widely; however, the effect of FGF-23 on the cardiovascular system (CVS) is unknown. To asse...

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Source

Identifiers

PMID: 19684183
DOI: 10.1152/ajpheart.00581.2009

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-19684183-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

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Hypophosphatemia-mediated hypotension in transgenic mice overexpressing human FGF-23.PMID 19684183Read ↗

Amelioration of the premature ageing-like features of Fgf-23 knockout mice by genetically restoring the systemic actions of FGF-23.Semantic proximity Read ↗

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

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Chronic inhibition of ERK1/2 signaling improves disordered bone and mineral metabolism in hypophosphatemic (Hyp) mice.Semantic proximity Read ↗

Hyperphosphatemia increases inflammation to exacerbate anemia and skeletal muscle wasting independently of FGF23-FGFR4 signalingSemantic proximity Read ↗

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