ArticleAmerican journal of physiology. Renal physiology2018
Acute blood loss stimulates fibroblast growth factor 23 production.
Article in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 63 citations in OpenAlex.
- Epoetin Beta and C-Terminal Fibroblast Growth Factor 23 in Patients With Chronic Heart Failure and Chronic Kidney Disease.Journal of the American Heart Association · 2019Trial
- Erythropoietin stimulates fibroblast growth factor 23 (FGF23) in mice and men.Pflugers Archiv : European journal of physiology · 2018Trial
- Broken signals: when the mineralostat alters the cardiovascular system.Pediatric nephrology (Berlin, Germany) · 2026Review
- Exploring the dynamics of FGF23 in patients with Hereditary Hemochromatosis type I following iron depletive treatment: a pilot study.Journal of endocrinological investigation · 2026Article
- A bone to pick with ferric carboxymaltose.Blood · 2026Article
- Anemia and Mineral Bone Disorder in Kidney Disease Patients: The Role of FGF-23 and Other Related Factors.International journal of molecular sciences · 2024Review
- Fibroblast growth factor 23 is pumping iron: C-terminal-fibroblast growth factor 23 cleaved peptide and its function in iron metabolism.Current opinion in nephrology and hypertension · 2024Review
- Non-Classical Effects of FGF23: Molecular and Clinical Features.International journal of molecular sciences · 2024Review
- Associations between anemia and FGF23 in the CKiD study.Pediatric nephrology (Berlin, Germany) · 2024Article
- Exploring endocrine FGFs - structures, functions and biomedical applications.International journal of biochemistry and molecular biology · 2024Review
- Article
- Bone marrow sinusoidal endothelial cells are a site of Fgf23 upregulation in a mouse model of iron deficiency anemia.Blood advances · 2023Article
- Bone-derived C-terminal FGF23 cleaved peptides increase iron availability in acute inflammation.Blood · 2023Article
- Fibroblast Growth Factor 23 Bone Regulation and Downstream Hormonal Activity.Calcified tissue international · 2023Review
- Interconnections of fibroblast growth factor 23 and klotho with erythropoietin and hypoxia-inducible factor.Molecular and cellular biochemistry · 2022Review
- Renoprotective effects of ferric citrate in a mouse model of chronic kidney disease.Scientific reports · 2022Article
- Crosstalk of fibroblast growth factor 23 and anemia-related factors during the development and progression of CKD (Review).Experimental and therapeutic medicine · 2021Review
- Associations among erythropoietic, iron-related, and FGF23 parameters in pediatric kidney transplant recipients.Pediatric nephrology (Berlin, Germany) · 2021Article
- C-Terminal, but Not Intact, FGF23 and EPO Are Strongly Correlatively Elevated in Patients With Gain-of-Function Mutations in HIF2A: Clinical Evidence for EPO Regulating FGF23.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- Upstream Regulators of Fibroblast Growth Factor 23.Frontiers in endocrinology · 2021Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Fibroblast growth factor 23 (FGF23) production is upregulated by iron deficiency and hypoxia. However, the influence of acute blood loss, and the resulting increases in circulating erythropoietin, on FGF23 production is unknown. Using wild-type C57BL/6 mice, we show that acute loss of 10% total blood volume leads to an increase in plasma C-terminal FGF23 (cFGF23) levels within 6 h, while plasma levels of intact FGF23, phosphate, calcium, parathyroid hormone, iron, and ferritin remain similar to control mice without acute blood loss. Volume resuscitation with PBS did not significantly alter these findings. The increase in plasma cFGF23 levels in bled animals was accompanied by increased plasma erythropoietin levels at 6 h. Administration of erythropoietin led to an acute increase in plasma cFGF23 levels similar to that observed in acute blood loss. Fgf23 mRNA expression was increased 20-fold in bone marrow, but not in bone, of bled vs. control mice, suggesting bone marrow as a key source of elevated plasma FGF23 levels following acute blood loss. To extend these findings to humans, we measured plasma cFGF23 levels in 131 critically ill patients admitted to the intensive care unit. In univariate and multivariate models, we found a positive association between number of red blood cell transfusions, an indirect indicator of acute blood loss, and plasma cFGF23 levels. We conclude that FGF23 production is rapidly increased after acute blood loss and that erythropoietin may be the mediator of this increase. Thus erythropoietin may represent a novel physiological regulator of FGF23 production.
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Registered trials
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 OpenQuestion graph.