ArticleMolecular metabolism2018
Phosphate-dependent FGF23 secretion is modulated by PiT2/Slc20a2.
Article in Molecular metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 84 citations in OpenAlex.
- Phosphate homeostasis and endocrine regulators.Pediatric nephrology (Berlin, Germany) · 2026Review
- Inhibition of FGFR signaling attenuates phosphaturia and early kidney injury in sickle cell disease mice.Biochemistry and biophysics reports · 2026Article
- FGF23 - A hormone produced by bone and has many faces.Reviews in endocrine & metabolic disorders · 2026Review
- Review
- Fibroblast growth factor 23: Regulation, signalling and systemic links between bone, metabolism and inflammation.Molecular metabolism · 2026Review
- Early-onset Fahr's disease with acute psychosis in a 20-year-old male with SLC20A2 mutation: A case report and literature review.Radiology case reports · 2026Article
- TGFβ signaling regulates the response of the skeleton to phosphate.bioRxiv : the preprint server for biology · 2025Article
- Characterisation of phosphate transport in epididymis and prostate with possible relevance for semen quality.EBioMedicine · 2025Article
- Osteoblasts sense extracellular levels of phosphate to control the local expression of phosphatases for matrix mineralisation.Bone reports · 2025Article
- Phosphate in Physiological and Pathological Mineralization: Important yet Often Unheeded.MedComm · 2025Review
- The role of fibroblast growth factor 23 in regulation of phosphate balance.Pediatric nephrology (Berlin, Germany) · 2024Review
- Influence of N- and/or P-restriction on bone metabolism in young goats.The British journal of nutrition · 2024Article
- Crosstalk between kidney and bone: insights from CKD-MBD.Journal of bone and mineral metabolism · 2024Review
- Organic phosphate but not inorganic phosphate regulatesiScience · 2024Article
- Gα11 deficiency increases fibroblast growth factor 23 levels in a mouse model of familial hypocalciuric hypercalcemia.JCI insight · 2024Article
- Phosphate in Cardiovascular Disease: From New Insights Into Molecular Mechanisms to Clinical Implications.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Pharmacology of Mammalian NaHandbook of experimental pharmacology · 2024Article
- Fibroblast Growth Factor 23 Neutralizing Antibody Ameliorates Abnormal Renal Phosphate Handling in Sickle Cell Disease Mice.Endocrinology · 2023Article
- Frontiers in Bone Metabolism and Disorder in Chronic Kidney Disease.Metabolites · 2023Article
- A prospective study of the association between serum klotho and mortality among adults with rheumatoid arthritis in the USA.Arthritis research & therapy · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe canonical role of the bone-derived fibroblast growth factor 23 (Fgf23) is to regulate the serum inorganic phosphate (Pi) level. As part of a feedback loop, serum Pi levels control Fgf23 secretion through undefined mechanisms. We recently showed in vitro that the two high-affinity Na
methodsTo this aim, we used PiT2 KO and DMP1Cre; PiT1
resultsIn vivo, PiT2 KO mice responded inappropriately to low-Pi diets, displaying abnormally normal serum levels of intact Fgf23. Despite the high iFgf23 level, serum Pi levels remained unaffected, an effect that may relate to lower αKlotho expression in the kidney. Moreover, consistent with a role of PiT2 as a possible endocrine Pi sensor, the iFGF23/cFGF23 ratios were suppressed in PiT2 KO mice, irrespective of the Pi loads. While deletion of PiT1 in osteocytes using the DMP1-Cre mice was inefficient, adenovirus-mediated deletion of PiT1 in isolated long bone shafts suggested that PiT1 does not contribute to Pi-dependent regulation of Fgf23 secretion. In contrast, using isolated bone shafts from PiT2 KO mice, we showed that PiT2 was necessary for the appropriate Pi-dependent secretion of Fgf23, independently from possible endocrine regulatory loops.
conclusionsOur data provide initial mechanistic insights underlying the Pi-dependent regulation of Fgf23 secretion in identifying PiT2 as a potential player in this process, at least in high Pi conditions. Targeting PiT2, therefore, could improve excess FGF23 in hyperphosphatemic conditions such as chronic kidney disease.
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