دورية أكاديمية
Glycerol-3-phosphate is an FGF23 regulator derived from the injured kidney.
العنوان: | Glycerol-3-phosphate is an FGF23 regulator derived from the injured kidney. |
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المؤلفون: | Simic P; Nephrology Division and.; Endocrine Unit, Endocrinology Division, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA., Kim W; Nephrology Division and.; Endocrine Unit, Endocrinology Division, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA., Zhou W; Nephrology Division and.; Endocrine Unit, Endocrinology Division, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA., Pierce KA; Broad Institute, Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts, USA., Chang W; Endocrine Research Unit, San Francisco Veterans Affairs Medical Center, UCSF, San Francisco, California, USA., Sykes DB; Center for Hematology, Cancer Center, and., Aziz NB; Center for Hematology, Cancer Center, and., Elmariah S; Cardiology Division, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA., Ngo D; Cardiovascular Research Center, Division of Cardiovascular Medicine, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA., Pajevic PD; Department of Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, Boston University, Boston, Massachusetts, USA., Govea N; Endocrine Unit, Endocrinology Division, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA., Kestenbaum BR; Kidney Research Institute, University of Washington Medicine and Northwest Kidney Centers, Seattle, Washington, USA., de Boer IH; Kidney Research Institute, University of Washington Medicine and Northwest Kidney Centers, Seattle, Washington, USA., Cheng Z; Endocrine Research Unit, San Francisco Veterans Affairs Medical Center, UCSF, San Francisco, California, USA., Christov M; Department of Medicine, New York Medical College, Touro College, Valhalla, New York, USA., Chun J; Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California, USA., Leaf DE; Division of Renal (Kidney) Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA., Waikar SS; Renal Section, Department of Medicine, Boston University Medical Center, Boston, Massachusetts, USA., Tager AM; Division of Pulmonary and Critical Care Medicine, Department of Medicine, and., Gerszten RE; Broad Institute, Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts, USA.; Cardiovascular Research Center, Division of Cardiovascular Medicine, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA., Thadhani RI; Nephrology Division and., Clish CB; Broad Institute, Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts, USA., Jüppner H; Endocrine Unit, Endocrinology Division, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA.; Pediatric Nephrology and Hypertension Program, Mass General for Children, Massachusetts General Hospital, Boston, Massachusetts, USA., Wein MN; Endocrine Unit, Endocrinology Division, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA., Rhee EP; Nephrology Division and.; Endocrine Unit, Endocrinology Division, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA.; Broad Institute, Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts, USA. |
المصدر: | The Journal of clinical investigation [J Clin Invest] 2020 Mar 02; Vol. 130 (3), pp. 1513-1526. |
نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
اللغة: | English |
بيانات الدورية: | Publisher: American Society for Clinical Investigation Country of Publication: United States NLM ID: 7802877 Publication Model: Print Cited Medium: Internet ISSN: 1558-8238 (Electronic) Linking ISSN: 00219738 NLM ISO Abbreviation: J Clin Invest Subsets: MEDLINE |
أسماء مطبوعة: | Publication: 1999- : Ann Arbor, MI : American Society for Clinical Investigation Original Publication: New Haven [etc.] American Society for Clinical Investigation. |
مواضيع طبية MeSH: | Acute Kidney Injury/*metabolism , Fibroblast Growth Factors/*metabolism , Glycerophosphates/*metabolism , Kidney/*metabolism, Acute Kidney Injury/genetics ; Acute Kidney Injury/pathology ; Animals ; Cell Line ; Female ; Fibroblast Growth Factor-23 ; Fibroblast Growth Factors/genetics ; Humans ; Kidney/pathology ; Male ; Metabolomics ; Mice ; Mice, Knockout ; Receptors, Lysophosphatidic Acid/genetics ; Receptors, Lysophosphatidic Acid/metabolism |
مستخلص: | 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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معلومات مُعتمدة: | K08 DK124568 United States DK NIDDK NIH HHS; P30 DK040561 United States DK NIDDK NIH HHS; R01 NR017399 United States NR NINR NIH HHS; R01 DK116716 United States DK NIDDK NIH HHS; R01 DK081572 United States DK NIDDK NIH HHS; R01 AR067291 United States AR NIAMS NIH HHS; I01 BX003453 United States BX BLRD VA; U01 DK106981 United States DK NIDDK NIH HHS; R01 HL132320 United States HL NHLBI NIH HHS; R01 DK122259 United States DK NIDDK NIH HHS; IK6 BX004835 United States BX BLRD VA; P01 DK011794 United States DK NIDDK NIH HHS; R01 HL133870 United States HL NHLBI NIH HHS; K08 AR067285 United States AR NIAMS NIH HHS |
فهرسة مساهمة: | Keywords: Bone Biology; Bone disease; Chronic kidney disease; Homeostasis; Nephrology |
المشرفين على المادة: | 0 (FGF23 protein, human) 0 (Fgf23 protein, mouse) 0 (Glycerophosphates) 0 (LPAR1 protein, human) 0 (Receptors, Lysophosphatidic Acid) 0 (lysophosphatidic acid receptor 1, mouse) 62031-54-3 (Fibroblast Growth Factors) 7Q7P4S7RRE (Fibroblast Growth Factor-23) 9NTI6P3O4X (alpha-glycerophosphoric acid) |
تواريخ الأحداث: | Date Created: 20200218 Date Completed: 20201103 Latest Revision: 20230504 |
رمز التحديث: | 20231215 |
مُعرف محوري في PubMed: | PMC7269595 |
DOI: | 10.1172/JCI131190 |
PMID: | 32065590 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1558-8238 |
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DOI: | 10.1172/JCI131190 |