ArticleThe Journal of clinical investigation2020
Glycerol-3-phosphate is an FGF23 regulator derived from the injured kidney.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
86 citing papers in PubMed, 120 citations in OpenAlex.
- FGF23 - A hormone produced by bone and has many faces.Reviews in endocrine & metabolic disorders · 2026Review
- Fibroblast growth factor-23 as an early biomarker of ischemic acute kidney injury after partial nephrectomy: prospective observational study.Scientific reports · 2026Observational
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Causal role of serum metabolites in chronic periodontitis: A bidirectional Mendelian randomization and multi-omics integration study.Medicine · 2026Article
- Broken signals: when the mineralostat alters the cardiovascular system.Pediatric nephrology (Berlin, Germany) · 2026Review
- Markers of Mineral Metabolism in Children With CKD Stages 2 to 5D.Kidney international reports · 2026Article
- The effects of elevated phosphate on the kidney - damaging the gatekeeper.Pflugers Archiv : European journal of physiology · 2026Review
- Aromatase: a new regulator of phosphate homeostasis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026Article
- Changes in bone characteristics precede serum mineral deterioration in a mouse model of early stage chronic kidney disease.JBMR plus · 2026Article
- Association between Serum Glycerol-3-Phosphate and Fibroblast Growth Factor-23 in Nondiabetic Patients on Hemodialysis.Clinical journal of the American Society of Nephrology : CJASN · 2026Article
- Bone mineral loss damages renal tubules in mice.Communications biology · 2026Article
- Lysophosphatidic Acid Synergizes With 1,25-Dihydroxyvitamin D to Promote Fibroblast Growth Factor-23 Synthesis via MAPK Signaling and Induction of the IL12A Gene.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Glycerol and Glycerol-3-Phosphate: Multifaceted Metabolites in Metabolism, Cancer, and Other Diseases.Endocrine reviews · 2026Review
- Gut microbiota in chronic kidney disease-mineral and bone disorder: shared mechanisms, disease-specific signatures, and therapeutic prospects.Frontiers in endocrinology · 2026Review
- Heterogeneous regulation of fibroblast growth factor 23 in acute kidney injury, chronic kidney disease, and polycystic kidney disease: mechanisms, diagnostic utility, and clinical implications.Frontiers in molecular biosciences · 2026Review
- TGFβ signaling regulates the response of the skeleton to phosphate.bioRxiv : the preprint server for biology · 2025Article
- The role of bone in whole-body energy metabolism.Nature reviews. Endocrinology · 2025Review
- Deletion of cardiac fibroblast growth factor-23 beneficially impacts myocardial energy metabolism in left ventricular hypertrophy.npj metabolic health and disease · 2025Article
- Decoding lysophosphatidic acid signaling in physiology and disease: mapping the multimodal and multinodal signaling networks.Signal transduction and targeted therapy · 2025Review
- Accelerated osteocytic citrate production in chronic kidney disease is associated with protection of the kidney.bioRxiv : the preprint server for biology · 2025Article
26 more citing papers are in PubMed but not listed here.
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25 authors at 12 institutions in 1 country.
Funding
Abstract
Fibroblast growth factor 23 (FGF23) is a bone-derived hormone that controls blood phosphate levels by increasing renal phosphate excretion and reducing 1,25-dihydroxyvitamin D3 [1,25(OH)2D] production. Disorders of FGF23 homeostasis are associated with significant morbidity and mortality, but a fundamental understanding of what regulates FGF23 production is lacking. Because the kidney is the major end organ of FGF23 action, we hypothesized that it releases a factor that regulates FGF23 synthesis. Using aptamer-based proteomics and liquid chromatography-mass spectrometry-based (LC-MS-based) metabolomics, we profiled more than 1600 molecules in renal venous plasma obtained from human subjects. Renal vein glycerol-3-phosphate (G-3-P) had the strongest correlation with circulating FGF23. In mice, exogenous G-3-P stimulated bone and bone marrow FGF23 production through local G-3-P acyltransferase-mediated (GPAT-mediated) lysophosphatidic acid (LPA) synthesis. Further, the stimulatory effect of G-3-P and LPA on FGF23 required LPA receptor 1 (LPAR1). Acute kidney injury (AKI), which increases FGF23 levels, rapidly increased circulating G-3-P in humans and mice, and the effect of AKI on FGF23 was abrogated by GPAT inhibition or Lpar1 deletion. Together, our findings establish a role for kidney-derived G-3-P in mineral metabolism and outline potential targets to modulate FGF23 production during kidney injury.
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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 Socratic graph.