Plasma fibroblast growth factor 23 and risk of cardiovascular disease: results from the EPIC-Germany case-cohort study

Giuseppe, Romina di; Kühn, Tilmann; Hirche, Frank; Buijsse, Brian; Dierkes, Jutta; Fritsche, Andreas; Kaaks, Rudolf; Boeing, Heiner; Stangl, Gabriele I.; Weikert, Cornelia

doi:10.1007/s10654-014-9982-4

Cited by 46 publications

(56 citation statements)

References 46 publications

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“…In addition to its phosphaturic and vitamin D hormone‐suppressive actions, FGF23 may have an important role for cardiovascular health. Several large epidemiological studies have linked increased circulating FGF23 with left ventricular mass and hypertrophy, impaired left ventricular function, vascular dysfunction, and increased risk for MI . In addition, it is well established that circulating FGF23 is positively and dose‐dependently associated with cardiovascular risk factors such as left ventricular hypertrophy, vascular calcifications, and mortality in patients with chronic kidney disease .…”

Section: Introductionmentioning

confidence: 99%

“…Several large epidemiological studies have linked increased circulating FGF23 with left ventricular mass and hypertrophy, impaired left ventricular function, vascular dysfunction, and increased risk for MI. (25)(26)(27)(28) In addition, it is well established that circulating FGF23 is positively and dose-dependently associated with cardiovascular risk factors such as left ventricular hypertrophy, vascular calcifications, and mortality in patients with chronic kidney disease. (29,30) Moreover, circulating FGF23 levels have been shown to independently predict clinical outcome in patients with established heart failure.…”

Section: Introductionmentioning

confidence: 99%

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Experimental Myocardial Infarction Upregulates Circulating Fibroblast Growth Factor-23

Andrukhova

Slavić

Odörfer

et al. 2015

Journal of Bone and Mineral Research

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Myocardial infarction (MI) is a major cause of death worldwide. Epidemiological studies have linked vitamin D deficiency to MI incidence. Because fibroblast growth factor‐23 (FGF23) is a master regulator of vitamin D hormone production and has been shown to be associated with cardiac hypertrophy per se, we explored the hypothesis that FGF23 may be a previously unrecognized pathophysiological factor causally linked to progression of cardiac dysfunction post‐MI. Here, we show that circulating intact Fgf23 was profoundly elevated, whereas serum vitamin D hormone levels were suppressed, after induction of experimental MI in rat and mouse models, independent of changes in serum soluble Klotho or serum parathyroid hormone. Both skeletal and cardiac expression of Fgf23 was increased after MI. Although the molecular link between the cardiac lesion and circulating Fgf23 concentrations remains to be identified, our study has uncovered a novel heart–bone–kidney axis that may have important clinical implications and may inaugurate the new field of cardio‐osteology. © 2015 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research (ASBMR).

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Experimental Myocardial Infarction Upregulates Circulating Fibroblast Growth Factor-23

Andrukhova

Slavić

Odörfer

et al. 2015

Journal of Bone and Mineral Research

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“…First, the study sample was relatively small. Second, it has been reported that FGF23 level may be higher among subjects with incident myocardial infarction 39) and patients with significant CAD present lower soluble concentrations of Klotho 40) . The current study population underwent chest MDCT under the clinical diagnosis or suspicion of coronary artery disease; therefore, our findings may not be applicable to the general population.…”

Section: Logistic Regression Analysis For the Association Between -Klmentioning

confidence: 99%

Gender Specific Association between Serum Fibroblast Growth Factor 23/α-Klotho and Coronary Artery and Aortic Valve Calcification

Morita

Takeda

Fujita

et al. 2015

J Atheroscler Thromb

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Aim: Fibroblast growth factor 23 (FGF23) and -Klotho have been recently identified to play a crucial role in calcium/phosphate metabolism. We herein investigated the possible relation between serum FGF23/ -Klotho levels and coronary artery calcification (CAC) and aortic valve calcification (AVC). Methods: Among subjects with diagnosed or suspected coronary artery disease (CAD), CAC and AVC were estimated via the Agatston score of 320-detector computed tomography images, and serum FGF23 and -Klotho levels were measured. Results: In total, 157 subjects were enrolled (75 women and 82 men). We performed logistic regression using CAC as a dependent variable; the highest FGF23 tertile ( 52.5 pg/mL) was significantly positively associated with CAC with an odds ratio of 6.61 versus the lowest FGF23 tertile ( 35.3 pg/mL) in women after the adjustment for potential confounding variables including age, renal function, hypertension, statin use, diuretic use, and calcium/phosphate metabolism related factors. In addition, the highest -Klotho tertile ( 561 pg/mL) was significantly associated with AVC with an odds ratio of 6.31 versus the lowest -Klotho tertile ( 306 pg/mL) in men after adjusting for the same variables. On the other hand, the association between FGF23 and CAC/AVC in men or that between -Klotho and CAC/AVC in women was nonsignificant. Conclusion: Among subjects with diagnosed or suspected CAD, serum FGF23 was positively associated with CAC in women and serum -Klotho was positively associated with AVC in men independent of the confounding variables, including the renal function and calcium/phosphate metabolismrelated factors. J Atheroscler Thromb, 2015; 22: 1338-1346.

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“…FGF23 was extensively studied in renal dysfunction and inflammation [6][7][8][9][10]. Recently, FGF23 was associated with atrial fibrillation, left ventricular hypertrophy, as well as morbidity and mortality in heart failure [5,11,12]. However, most studies of FGF23 and heart failure are confounded by chronic kidney disease which is accompanied by disturbed mineral-, blood and Iron-homeostasis as well as inflammationall of them interacting with FGF23making it difficult to explain a direct role of FGF23 on the heart [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

The Association of Fgf23 and Inflammation in Heart Failure with Normal Kidney Function

Ulmer¹,

Koller²,

Dörler³

et al. 2019

JICOA

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Keywords:Fibrosing growth factor23 C-reactive protein heart failure cardiomyopathy subclinical inflammation biomarkers A B S T R A C T Background: Fibroblast growth factor-23 produced by osteocytes regulates calcium and phosphate homeostasis which are cornerstones for bone integrity. Recently, FGF23 was also found to be directly related with both severity and prognosis of heart failure. However, the mechanism of FGF23 regulation in heart failure, particularly in patients with preserved renal function is poorly understood. Methods:In this retrospective single center trial we assessed the association of systemic inflammation (surrogated by CRP) and FGF23 regulation in 221 stable non-ischemic heart failure patients (age ≥ 18) with reduced ejection fraction and an estimated glomerular filtration rate of more than 60 ml/min/1.73m². Furthermore, we analyzed the prognostic ability of FGF23 and CRP in this population. Fasting ct-FGF23, highly sensitive CRP and a comprehensive panel of further biomarkers, as well as invasive hemodynamic measures from right heart catheterization, were used for univariate and multivariate regression analysis. Results:In bivariate correlation analysis ct-FGF23 was correlated with Cardiac output (r= -0.42); NTproBNP (r=0.34) and CRP (r=0.31); for all of those p < 0.001. Multivariate linear regression analysis revealed CRP and CO as independently associated with ct-FGF23 (total model fit; r²=0.32; p <0.001). In time to event analysis ct-FGF23 was the only independent parameter predicting transplant-free survival. Conclusion:Our data indicate an association of systemic inflammation and FGF23 in heart failure independent from renal function and supports the hypothesis that FGF23 may be directly involved in heart failure. 10. Manghat P, Fraser WD, Wierzbicki AS, Fogelman I, Goldsmith DJ et al. (2010) Fibroblast growth factor-23 is associated with C-reactive protein, serum phosphate and bone mineral density in chronic kidney disease.

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Plasma fibroblast growth factor 23 and risk of cardiovascular disease: results from the EPIC-Germany case-cohort study

Cited by 46 publications

References 46 publications

Experimental Myocardial Infarction Upregulates Circulating Fibroblast Growth Factor-23

Experimental Myocardial Infarction Upregulates Circulating Fibroblast Growth Factor-23

Gender Specific Association between Serum Fibroblast Growth Factor 23/α-Klotho and Coronary Artery and Aortic Valve Calcification

The Association of Fgf23 and Inflammation in Heart Failure with Normal Kidney Function

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