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 in | Frontiers in physiology Vol. 12; p. 632260 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Frontiers Media S.A
09.03.2021
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Subjects | |
Online Access | Get full text |
ISSN | 1664-042X 1664-042X |
DOI | 10.3389/fphys.2021.632260 |
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Summary: | 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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 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 |
ISSN: | 1664-042X 1664-042X |
DOI: | 10.3389/fphys.2021.632260 |