An Overview of FGF-23 as a Novel Candidate Biomarker of Cardiovascular Risk

Fibroblast growth factor-23 (FGF)-23 is a phosphaturic hormone involved in mineral bone metabolism that helps control phosphate homeostasis and reduces 1,25-dihydroxyvitamin D synthesis. Recent data have highlighted the relevant direct FGF-23 effects on the myocardium, and high plasma levels of FGF-...

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Published inFrontiers in physiology Vol. 12; p. 632260
Main Authors Vázquez-Sánchez, Sara, Poveda, Jonay, Navarro-García, José Alberto, González-Lafuente, Laura, Rodríguez-Sánchez, Elena, Ruilope, Luis M., Ruiz-Hurtado, Gema
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 09.03.2021
Subjects
FGF-23
FGFR
heart
heart failure – pharmacological treatment – systolic dysfunction
LVH
Physiology
heart failure – pharmacological treatment – systolic dysfunction
FGF-23
FGFR
heart
LVH
Online AccessGet full text
ISSN1664-042X
1664-042X
DOI10.3389/fphys.2021.632260

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Abstract Fibroblast growth factor-23 (FGF)-23 is a phosphaturic hormone involved in mineral bone metabolism that helps control phosphate homeostasis and reduces 1,25-dihydroxyvitamin D synthesis. Recent data have highlighted the relevant direct FGF-23 effects on the myocardium, and high plasma levels of FGF-23 have been associated with adverse cardiovascular outcomes in humans, such as heart failure and arrhythmias. Therefore, FGF-23 has emerged as a novel biomarker of cardiovascular risk in the last decade. Indeed, experimental data suggest FGF-23 as a direct mediator of cardiac hypertrophy development, cardiac fibrosis and cardiac dysfunction via specific myocardial FGF receptor (FGFR) activation. Therefore, the FGF-23/FGFR pathway might be a suitable therapeutic target for reducing the deleterious effects of FGF-23 on the cardiovascular system. More research is needed to fully understand the intracellular FGF-23-dependent mechanisms, clarify the downstream pathways and identify which could be the most appropriate targets for better therapeutic intervention. This review updates the current knowledge on both clinical and experimental studies and highlights the evidence linking FGF-23 to cardiovascular events. The aim of this review is to establish the specific role of FGF-23 in the heart, its detrimental effects on cardiac tissue and the possible new therapeutic opportunities to block these effects.
AbstractList Fibroblast growth factor-23 (FGF)-23 is a phosphaturic hormone involved in mineral bone metabolism that helps control phosphate homeostasis and reduces 1,25-dihydroxyvitamin D synthesis. Recent data have highlighted the relevant direct FGF-23 effects on the myocardium, and high plasma levels of FGF-23 have been associated with adverse cardiovascular outcomes in humans, such as heart failure and arrhythmias. Therefore, FGF-23 has emerged as a novel biomarker of cardiovascular risk in the last decade. Indeed, experimental data suggest FGF-23 as a direct mediator of cardiac hypertrophy development, cardiac fibrosis and cardiac dysfunction via specific myocardial FGF receptor (FGFR) activation. Therefore, the FGF-23/FGFR pathway might be a suitable therapeutic target for reducing the deleterious effects of FGF-23 on the cardiovascular system. More research is needed to fully understand the intracellular FGF-23-dependent mechanisms, clarify the downstream pathways and identify which could be the most appropriate targets for better therapeutic intervention. This review updates the current knowledge on both clinical and experimental studies and highlights the evidence linking FGF-23 to cardiovascular events. The aim of this review is to establish the specific role of FGF-23 in the heart, its detrimental effects on cardiac tissue and the possible new therapeutic opportunities to block these effects.
Fibroblast growth factor-23 (FGF)-23 is a phosphaturic hormone involved in mineral bone metabolism that helps control phosphate homeostasis and reduces 1,25-dihydroxyvitamin D synthesis. Recent data have highlighted the relevant direct FGF-23 effects on the myocardium, and high plasma levels of FGF-23 have been associated with adverse cardiovascular outcomes in humans, such as heart failure and arrhythmias. Therefore, FGF-23 has emerged as a novel biomarker of cardiovascular risk in the last decade. Indeed, experimental data suggest FGF-23 as a direct mediator of cardiac hypertrophy development, cardiac fibrosis and cardiac dysfunction via specific myocardial FGF receptor (FGFR) activation. Therefore, the FGF-23/FGFR pathway might be a suitable therapeutic target for reducing the deleterious effects of FGF-23 on the cardiovascular system. More research is needed to fully understand the intracellular FGF-23-dependent mechanisms, clarify the downstream pathways and identify which could be the most appropriate targets for better therapeutic intervention. This review updates the current knowledge on both clinical and experimental studies and highlights the evidence linking FGF-23 to cardiovascular events. The aim of this review is to establish the specific role of FGF-23 in the heart, its detrimental effects on cardiac tissue and the possible new therapeutic opportunities to block these effects.Fibroblast growth factor-23 (FGF)-23 is a phosphaturic hormone involved in mineral bone metabolism that helps control phosphate homeostasis and reduces 1,25-dihydroxyvitamin D synthesis. Recent data have highlighted the relevant direct FGF-23 effects on the myocardium, and high plasma levels of FGF-23 have been associated with adverse cardiovascular outcomes in humans, such as heart failure and arrhythmias. Therefore, FGF-23 has emerged as a novel biomarker of cardiovascular risk in the last decade. Indeed, experimental data suggest FGF-23 as a direct mediator of cardiac hypertrophy development, cardiac fibrosis and cardiac dysfunction via specific myocardial FGF receptor (FGFR) activation. Therefore, the FGF-23/FGFR pathway might be a suitable therapeutic target for reducing the deleterious effects of FGF-23 on the cardiovascular system. More research is needed to fully understand the intracellular FGF-23-dependent mechanisms, clarify the downstream pathways and identify which could be the most appropriate targets for better therapeutic intervention. This review updates the current knowledge on both clinical and experimental studies and highlights the evidence linking FGF-23 to cardiovascular events. The aim of this review is to establish the specific role of FGF-23 in the heart, its detrimental effects on cardiac tissue and the possible new therapeutic opportunities to block these effects.
Author Rodríguez-Sánchez, Elena
Vázquez-Sánchez, Sara
Ruiz-Hurtado, Gema
Navarro-García, José Alberto
González-Lafuente, Laura
Poveda, Jonay
Ruilope, Luis M.
AuthorAffiliation 1 Cardiorenal Translational Laboratory, Institute of Research i+12, Hospital Universitario 12 de Octubre , Madrid , Spain
2 CIBER-CV, Hospital Universitario 12 de Octubre , Madrid , Spain
3 School of Doctoral Studies and Research, European University of Madrid , Madrid , Spain
AuthorAffiliation_xml – name: 1 Cardiorenal Translational Laboratory, Institute of Research i+12, Hospital Universitario 12 de Octubre , Madrid , Spain
– name: 3 School of Doctoral Studies and Research, European University of Madrid , Madrid , Spain
– name: 2 CIBER-CV, Hospital Universitario 12 de Octubre , Madrid , Spain
Author_xml – sequence: 1
  givenname: Sara
  surname: Vázquez-Sánchez
  fullname: Vázquez-Sánchez, Sara
– sequence: 2
  givenname: Jonay
  surname: Poveda
  fullname: Poveda, Jonay
– sequence: 3
  givenname: José Alberto
  surname: Navarro-García
  fullname: Navarro-García, José Alberto
– sequence: 4
  givenname: Laura
  surname: González-Lafuente
  fullname: González-Lafuente, Laura
– sequence: 5
  givenname: Elena
  surname: Rodríguez-Sánchez
  fullname: Rodríguez-Sánchez, Elena
– sequence: 6
  givenname: Luis M.
  surname: Ruilope
  fullname: Ruilope, Luis M.
– sequence: 7
  givenname: Gema
  surname: Ruiz-Hurtado
  fullname: Ruiz-Hurtado, Gema
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33767635$$D View this record in MEDLINE/PubMed
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Copyright Copyright © 2021 Vázquez-Sánchez, Poveda, Navarro-García, González-Lafuente, Rodríguez-Sánchez, Ruilope and Ruiz-Hurtado.
Copyright © 2021 Vázquez-Sánchez, Poveda, Navarro-García, González-Lafuente, Rodríguez-Sánchez, Ruilope and Ruiz-Hurtado. 2021 Vázquez-Sánchez, Poveda, Navarro-García, González-Lafuente, Rodríguez-Sánchez, Ruilope and Ruiz-Hurtado
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Keywords heart failure – pharmacological treatment – systolic dysfunction
FGF-23
FGFR
heart
LVH
Language English
License Copyright © 2021 Vázquez-Sánchez, Poveda, Navarro-García, González-Lafuente, Rodríguez-Sánchez, Ruilope and Ruiz-Hurtado.
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Edited by: Modar Kassan, University of Tennessee Health Science Center (UTHSC), United States
Reviewed by: Ebba Brakenhielm, Institut National de la Santé et de la Recherche Médicale (INSERM), France; Akira Nishiyama, Kagawa University, Japan
These authors have contributed equally to this work
This article was submitted to Vascular Physiology, a section of the journal Frontiers in Physiology
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SubjectTerms FGF-23
FGFR
heart
heart failure – pharmacological treatment – systolic dysfunction
LVH
Physiology
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