Direct and indirect effects of fibroblast growth factor 23 on the heart
Fibroblast growth factor (FGF)23 is a bone-derived phosphotropic hormone that regulates phosphate and mineral homeostasis. Recent studies have provided evidence that a high plasma concentration of FGF23 is associated with cardiac disease, including left ventricular hypertrophy (LVH), heart failure,...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2023-02-01
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| Series: | Frontiers in Endocrinology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fendo.2023.1059179/full |
| _version_ | 1797895368021639168 |
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| author | Toshiaki Nakano Toshiaki Nakano Hiroshi Kishimoto Masanori Tokumoto |
| author_facet | Toshiaki Nakano Toshiaki Nakano Hiroshi Kishimoto Masanori Tokumoto |
| author_sort | Toshiaki Nakano |
| collection | DOAJ |
| description | Fibroblast growth factor (FGF)23 is a bone-derived phosphotropic hormone that regulates phosphate and mineral homeostasis. Recent studies have provided evidence that a high plasma concentration of FGF23 is associated with cardiac disease, including left ventricular hypertrophy (LVH), heart failure, atrial fibrillation, and cardiac death. Experimental studies have shown that FGF23 activates fibroblast growth factor receptor 4 (FGFR4)/phospholipase Cγ/calcineurin/nuclear factor of activated T-cells signaling in cardiomyocytes and induces cardiac hypertrophy in rodents. Activation of FGFR4 by FGF23 normally requires the co-receptor α-klotho, and klotho-independent signaling occurs only under conditions characterized by extremely high FGF23 concentrations. Recent studies have demonstrated that FGF23 activates the renin-angiotensin-aldosterone system (RAAS) and induces LVH, at least in part as a result of lower vitamin D activation. Moreover, crosstalk between FGF23 and RAAS results in the induction of cardiac hypertrophy and fibrosis. In this review, we summarize the results of studies regarding the relationships between FGF23 and cardiac events, and describe the potential direct and indirect mechanisms whereby FGF23 induces LVH. |
| first_indexed | 2024-04-10T07:24:25Z |
| format | Article |
| id | doaj.art-bf1dc357267a476096c3230761fda3a3 |
| institution | Directory Open Access Journal |
| issn | 1664-2392 |
| language | English |
| last_indexed | 2024-04-10T07:24:25Z |
| publishDate | 2023-02-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Endocrinology |
| spelling | doaj.art-bf1dc357267a476096c3230761fda3a32023-02-24T09:09:42ZengFrontiers Media S.A.Frontiers in Endocrinology1664-23922023-02-011410.3389/fendo.2023.10591791059179Direct and indirect effects of fibroblast growth factor 23 on the heartToshiaki Nakano0Toshiaki Nakano1Hiroshi Kishimoto2Masanori Tokumoto3Center for Cohort Studies, Graduate School of Medical Sciences, Kyushu University, Fukuoka, JapanDepartment of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, JapanDepartment of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, JapanDepartment of Nephrology, Fukuoka Red Cross Hospital, Fukuoka, JapanFibroblast growth factor (FGF)23 is a bone-derived phosphotropic hormone that regulates phosphate and mineral homeostasis. Recent studies have provided evidence that a high plasma concentration of FGF23 is associated with cardiac disease, including left ventricular hypertrophy (LVH), heart failure, atrial fibrillation, and cardiac death. Experimental studies have shown that FGF23 activates fibroblast growth factor receptor 4 (FGFR4)/phospholipase Cγ/calcineurin/nuclear factor of activated T-cells signaling in cardiomyocytes and induces cardiac hypertrophy in rodents. Activation of FGFR4 by FGF23 normally requires the co-receptor α-klotho, and klotho-independent signaling occurs only under conditions characterized by extremely high FGF23 concentrations. Recent studies have demonstrated that FGF23 activates the renin-angiotensin-aldosterone system (RAAS) and induces LVH, at least in part as a result of lower vitamin D activation. Moreover, crosstalk between FGF23 and RAAS results in the induction of cardiac hypertrophy and fibrosis. In this review, we summarize the results of studies regarding the relationships between FGF23 and cardiac events, and describe the potential direct and indirect mechanisms whereby FGF23 induces LVH.https://www.frontiersin.org/articles/10.3389/fendo.2023.1059179/fullFGF23HeartLeft ventricle hypertrophyFGFR4cardiac event |
| spellingShingle | Toshiaki Nakano Toshiaki Nakano Hiroshi Kishimoto Masanori Tokumoto Direct and indirect effects of fibroblast growth factor 23 on the heart Frontiers in Endocrinology FGF23 Heart Left ventricle hypertrophy FGFR4 cardiac event |
| title | Direct and indirect effects of fibroblast growth factor 23 on the heart |
| title_full | Direct and indirect effects of fibroblast growth factor 23 on the heart |
| title_fullStr | Direct and indirect effects of fibroblast growth factor 23 on the heart |
| title_full_unstemmed | Direct and indirect effects of fibroblast growth factor 23 on the heart |
| title_short | Direct and indirect effects of fibroblast growth factor 23 on the heart |
| title_sort | direct and indirect effects of fibroblast growth factor 23 on the heart |
| topic | FGF23 Heart Left ventricle hypertrophy FGFR4 cardiac event |
| url | https://www.frontiersin.org/articles/10.3389/fendo.2023.1059179/full |
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