ArticleScientific reports2022
Tmem174, a regulator of phosphate transporter prevents hyperphosphatemia.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Review
- TMEM174 Deficiency Reduces Longevity by Promoting Phosphate-Driven Vascular Calcification.Research square · 2026Article
- TMEM174 Deficiency Reduces Longevity by Promoting Phosphate-Driven Vascular Calcification.bioRxiv : the preprint server for biology · 2026Article
- PDZ domain containing protein 1 aggravates mouse vascular smooth muscle cells calcification via PDZ1 domain mediated β-catenin stabilization and nuclear translocation.Communications biology · 2025Article
- Identification of a risk model for prognostic and therapeutic prediction in renal cell carcinoma based on infiltrating M0 cells.Scientific reports · 2024Article
- Involvement of α-klotho in growth hormone (GH) signaling.Journal of clinical biochemistry and nutrition · 2024Article
- The molecular sociology of NHERF1 PDZ proteins controlling renal hormone-regulated phosphate transport.Bioscience reports · 2024Article
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Authors and funding
16 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Renal type II sodium-dependent inorganic phosphate (Pi) transporters NaPi2a and NaPi2c cooperate with other organs to strictly regulate the plasma Pi concentration. A high Pi load induces expression and secretion of the phosphaturic hormones parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) that enhance urinary Pi excretion and prevent the onset of hyperphosphatemia. How FGF23 secretion from bone is increased by a high Pi load and the setpoint of the plasma Pi concentration, however, are unclear. Here, we investigated the role of Transmembrane protein 174 (Tmem174) and observed evidence for gene co-expression networks in NaPi2a and NaPi2c function. Tmem174 is localized in the renal proximal tubules and interacts with NaPi2a, but not NaPi2c. In Tmem174-knockout (KO) mice, the serum FGF23 concentration was markedly increased but increased Pi excretion and hypophosphatemia were not observed. In addition, Tmem174-KO mice exhibit reduced NaPi2a responsiveness to FGF23 and PTH administration. Furthermore, a dietary Pi load causes marked hyperphosphatemia and abnormal NaPi2a regulation in Tmem174-KO mice. Thus, Tmem174 is thought to be associated with FGF23 induction in bones and the regulation of NaPi2a to prevent an increase in the plasma Pi concentration due to a high Pi load and kidney injury.
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