Deterioration of Phosphate Homeostasis Is a Trigger for Cardiac Afterload ― Clinical Importance of Fibroblast Growth Factor 23 for Accelerated Aging
Background: After the discovery of the Klotho gene, phosphate came into focus as a pathogenetic aging agent. Phosphate homeostasis is controlled by phosphate-regulating hormones: fibroblast growth factor 23 (FGF23), vitamin D3, and parathyroid hormone. This study investigated the relationship betwee...
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Published in | Circulation Reports Vol. 5; no. 1; pp. 4 - 12 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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Japan
The Japanese Circulation Society
10.01.2023
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Online Access | Get full text |
ISSN | 2434-0790 2434-0790 |
DOI | 10.1253/circrep.CR-22-0124 |
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Abstract | Background: After the discovery of the Klotho gene, phosphate came into focus as a pathogenetic aging agent. Phosphate homeostasis is controlled by phosphate-regulating hormones: fibroblast growth factor 23 (FGF23), vitamin D3, and parathyroid hormone. This study investigated the relationship between the deterioration in phosphate homeostasis and arterial stiffness by measuring serum FGF23 concentrations.Methods and Results: The study subjects comprised 82 hospitalized patients (31 males, 51 females; mean [±SD] age 78.6±10.5 years). All patients underwent chest computed tomography, measurement of central blood pressure (BP), and blood chemistry tests. Arterial calcification and/or stiffness was evaluated using the Agatston calcification score (ACS) and pulse wave velocity (PWV). PWV was significantly correlated with age (t=23.47, P<0.0001), estimated glomerular filtration rate (eGFR; t=−4.40, P<0.0001), and ACS (t=4.36, P<0.0001). Serum FGF23 concentrations were significantly correlated with age (t=2.52, P=0.014), eGFR (t=−3.37, P<0.001), serum inorganic phosphorus concentrations (t=3.49, P<0.001), serum vitamin D3concentrations (t=−4.57, P<0.001), ACS (t=2.30, P=0.025), augmentation pressure (t=2.48, P=0.015), central systolic BP (t=2.00, P=0.049), plasma B-type natriuretic peptide (BNP) concentrations (t=3.48, P<0.001), and PWV (t=2.99, P=0.004). PWV was positively related to augmentation pressure (t=4.09, P<0.001), central systolic BP (t=3.13, P=0.002), and plasma BNP concentrations (t=3.54, P<0.001).Conclusions: This study shows that the increase in serum FGF23 concentrations reflects deterioration of phosphate homeostasis and is an important predictor for arterial stiffness, which intensifies cardiac afterload. |
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AbstractList | Background: After the discovery of the Klotho gene, phosphate came into focus as a pathogenetic aging agent. Phosphate homeostasis is controlled by phosphate-regulating hormones: fibroblast growth factor 23 (FGF23), vitamin D3, and parathyroid hormone. This study investigated the relationship between the deterioration in phosphate homeostasis and arterial stiffness by measuring serum FGF23 concentrations. Methods and Results: The study subjects comprised 82 hospitalized patients (31 males, 51 females; mean [±SD] age 78.6±10.5 years). All patients underwent chest computed tomography, measurement of central blood pressure (BP), and blood chemistry tests. Arterial calcification and/or stiffness was evaluated using the Agatston calcification score (ACS) and pulse wave velocity (PWV). PWV was significantly correlated with age (t=23.47, P<0.0001), estimated glomerular filtration rate (eGFR; t=-4.40, P<0.0001), and ACS (t=4.36, P<0.0001). Serum FGF23 concentrations were significantly correlated with age (t=2.52, P=0.014), eGFR (t=-3.37, P<0.001), serum inorganic phosphorus concentrations (t=3.49, P<0.001), serum vitamin D3 concentrations (t=-4.57, P<0.001), ACS (t=2.30, P=0.025), augmentation pressure (t=2.48, P=0.015), central systolic BP (t=2.00, P=0.049), plasma B-type natriuretic peptide (BNP) concentrations (t=3.48, P<0.001), and PWV (t=2.99, P=0.004). PWV was positively related to augmentation pressure (t=4.09, P<0.001), central systolic BP (t=3.13, P=0.002), and plasma BNP concentrations (t=3.54, P<0.001). Conclusions: This study shows that the increase in serum FGF23 concentrations reflects deterioration of phosphate homeostasis and is an important predictor for arterial stiffness, which intensifies cardiac afterload.Background: After the discovery of the Klotho gene, phosphate came into focus as a pathogenetic aging agent. Phosphate homeostasis is controlled by phosphate-regulating hormones: fibroblast growth factor 23 (FGF23), vitamin D3, and parathyroid hormone. This study investigated the relationship between the deterioration in phosphate homeostasis and arterial stiffness by measuring serum FGF23 concentrations. Methods and Results: The study subjects comprised 82 hospitalized patients (31 males, 51 females; mean [±SD] age 78.6±10.5 years). All patients underwent chest computed tomography, measurement of central blood pressure (BP), and blood chemistry tests. Arterial calcification and/or stiffness was evaluated using the Agatston calcification score (ACS) and pulse wave velocity (PWV). PWV was significantly correlated with age (t=23.47, P<0.0001), estimated glomerular filtration rate (eGFR; t=-4.40, P<0.0001), and ACS (t=4.36, P<0.0001). Serum FGF23 concentrations were significantly correlated with age (t=2.52, P=0.014), eGFR (t=-3.37, P<0.001), serum inorganic phosphorus concentrations (t=3.49, P<0.001), serum vitamin D3 concentrations (t=-4.57, P<0.001), ACS (t=2.30, P=0.025), augmentation pressure (t=2.48, P=0.015), central systolic BP (t=2.00, P=0.049), plasma B-type natriuretic peptide (BNP) concentrations (t=3.48, P<0.001), and PWV (t=2.99, P=0.004). PWV was positively related to augmentation pressure (t=4.09, P<0.001), central systolic BP (t=3.13, P=0.002), and plasma BNP concentrations (t=3.54, P<0.001). Conclusions: This study shows that the increase in serum FGF23 concentrations reflects deterioration of phosphate homeostasis and is an important predictor for arterial stiffness, which intensifies cardiac afterload. After the discovery of the Klotho gene, phosphate came into focus as a pathogenetic aging agent. Phosphate homeostasis is controlled by phosphate-regulating hormones: fibroblast growth factor 23 (FGF23), vitamin D , and parathyroid hormone. This study investigated the relationship between the deterioration in phosphate homeostasis and arterial stiffness by measuring serum FGF23 concentrations. The study subjects comprised 82 hospitalized patients (31 males, 51 females; mean [±SD] age 78.6±10.5 years). All patients underwent chest computed tomography, measurement of central blood pressure (BP), and blood chemistry tests. Arterial calcification and/or stiffness was evaluated using the Agatston calcification score (ACS) and pulse wave velocity (PWV). PWV was significantly correlated with age (t=23.47, P<0.0001), estimated glomerular filtration rate (eGFR; t=-4.40, P<0.0001), and ACS (t=4.36, P<0.0001). Serum FGF23 concentrations were significantly correlated with age (t=2.52, P=0.014), eGFR (t=-3.37, P<0.001), serum inorganic phosphorus concentrations (t=3.49, P<0.001), serum vitamin D concentrations (t=-4.57, P<0.001), ACS (t=2.30, P=0.025), augmentation pressure (t=2.48, P=0.015), central systolic BP (t=2.00, P=0.049), plasma B-type natriuretic peptide (BNP) concentrations (t=3.48, P<0.001), and PWV (t=2.99, P=0.004). PWV was positively related to augmentation pressure (t=4.09, P<0.001), central systolic BP (t=3.13, P=0.002), and plasma BNP concentrations (t=3.54, P<0.001). This study shows that the increase in serum FGF23 concentrations reflects deterioration of phosphate homeostasis and is an important predictor for arterial stiffness, which intensifies cardiac afterload. Background: After the discovery of the Klotho gene, phosphate came into focus as a pathogenetic aging agent. Phosphate homeostasis is controlled by phosphate-regulating hormones: fibroblast growth factor 23 (FGF23), vitamin D3, and parathyroid hormone. This study investigated the relationship between the deterioration in phosphate homeostasis and arterial stiffness by measuring serum FGF23 concentrations.Methods and Results: The study subjects comprised 82 hospitalized patients (31 males, 51 females; mean [±SD] age 78.6±10.5 years). All patients underwent chest computed tomography, measurement of central blood pressure (BP), and blood chemistry tests. Arterial calcification and/or stiffness was evaluated using the Agatston calcification score (ACS) and pulse wave velocity (PWV). PWV was significantly correlated with age (t=23.47, P<0.0001), estimated glomerular filtration rate (eGFR; t=−4.40, P<0.0001), and ACS (t=4.36, P<0.0001). Serum FGF23 concentrations were significantly correlated with age (t=2.52, P=0.014), eGFR (t=−3.37, P<0.001), serum inorganic phosphorus concentrations (t=3.49, P<0.001), serum vitamin D3concentrations (t=−4.57, P<0.001), ACS (t=2.30, P=0.025), augmentation pressure (t=2.48, P=0.015), central systolic BP (t=2.00, P=0.049), plasma B-type natriuretic peptide (BNP) concentrations (t=3.48, P<0.001), and PWV (t=2.99, P=0.004). PWV was positively related to augmentation pressure (t=4.09, P<0.001), central systolic BP (t=3.13, P=0.002), and plasma BNP concentrations (t=3.54, P<0.001).Conclusions: This study shows that the increase in serum FGF23 concentrations reflects deterioration of phosphate homeostasis and is an important predictor for arterial stiffness, which intensifies cardiac afterload. |
ArticleNumber | CR-22-0124 |
Author | Kugimiya, Fumihito Nakayama, Yoshiharu Ishida, Toshifumi Yonemitsu, Koichiro Harada, Eisaku Mizuno, Yuji Takai, Seiko |
Author_xml | – sequence: 1 fullname: Yonemitsu, Koichiro organization: Division of Emergency Room, Kumamoto Kinoh Hospital – sequence: 1 fullname: Ishida, Toshifumi organization: Department of Cardiovascular Medicine, Faculty of Life Science, Graduate School of Medical Sciences, Kumamoto University – sequence: 1 fullname: Takai, Seiko organization: Division of Orthopedics, Kumamoto Kinoh Hospital – sequence: 1 fullname: Harada, Eisaku organization: Division of Cardiovascular Medicine, Kumamoto Kinoh Hospital – sequence: 1 fullname: Kugimiya, Fumihito organization: Division of Cardiovascular Medicine, Kumamoto Kinoh Hospital – sequence: 1 fullname: Mizuno, Yuji organization: Division of Cardiovascular Medicine, Mizuno Heart Clinic – sequence: 1 fullname: Nakayama, Yoshiharu organization: Division of Radiology Imaging, Kumamoto Kinoh Hospital |
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Cites_doi | 10.1038/ki.2012.327 10.1177/000456329703400606 10.1097/MBP.0b013e328339be38 10.1253/circj.CJ-14-0735 10.1007/s11154-011-9199-8 10.1038/srep24879 10.1097/HJH.0b013e3282f62a9b 10.1038/s41598-020-77308-3 10.1161/CIRCULATIONAHA.107.706127 10.1124/jpet.117.247270 10.1097/MBP.0b013e328338892f 10.1172/JCI15219 10.1359/jbmr.2001.16.4.605 10.1097/HJH.0000000000001406 10.1016/j.mad.2010.02.008 10.18632/aging.102297 10.3390/nu10050652 10.1146/annurev.med.051308.111339 10.1253/circj.CJ-08-0308 10.1016/j.jacbts.2020.02.002 10.4103/jcecho.jcecho_82_17 10.1016/j.acra.2007.05.021 10.1161/01.ATV.0000160548.78317.29 10.5551/jat.RV17045 10.1016/j.kint.2019.10.019 10.1007/s00424-018-2231-z 10.1161/hy1201.098767 10.1097/QAD.0000000000002414 10.1161/CIRCULATIONAHA.113.002654 10.1038/36285 10.1210/jc.2002-021105 10.1161/01.ATV.0000133194.94939.42 |
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Keywords | Calcification Arterial stiffness Fibroblast growth factor 23 Phosphate Afterload |
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References_xml | – reference: 20. Kunishige R, Mizoguchi M, Tsubouchi A, Hanaoka K, Miura Y, Kurosu H, et al. Calciprotein particle-induced cytotoxicity via lysosomal dysfunction and altered cholesterol distribution in renal epithelial HK-2 cells. Sci Rep 2020; 10: 20125, doi:10.1038/s41598-020-77308-3. – reference: 28. Li YC, Kong J, Wei M, Chen ZF, Liu SQ, Cao LP. 1,25-Dihydroxyvitamin D(3) is a negative endocrine regulator of the renin-angiotensin system. J Clin Invest 2002; 110: 229–238, doi:10.1172/jci15219. – reference: 2. Nelson AJ, Raggi P, Wolf M, Gold AM, Chertow GM, Roe MT. Targeting vascular calcification in chronic kidney disease. JACC Basic Transl Sci 2020; 5: 398–412, doi:10.1016/j.jacbts.2020.02.002. – reference: 7. Ärnlöv J, Carlsson AC, Sundström J, Ingelsson E, Larsson A, Lind L, et al. Higher fibroblast growth factor-23 increases the risk of all-cause and cardiovascular mortality in the community. 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Snippet | Background: After the discovery of the Klotho gene, phosphate came into focus as a pathogenetic aging agent. Phosphate homeostasis is controlled by... After the discovery of the Klotho gene, phosphate came into focus as a pathogenetic aging agent. Phosphate homeostasis is controlled by phosphate-regulating... |
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SubjectTerms | Afterload Arterial stiffness Calcification Fibroblast growth factor 23 Phosphate |
Title | Deterioration of Phosphate Homeostasis Is a Trigger for Cardiac Afterload ― Clinical Importance of Fibroblast Growth Factor 23 for Accelerated Aging |
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