Fibroblast Growth Factor-23 Is Associated With Disease Severity and Prognosis in Chronic Heart Failure

Poelzl, Gerhard; Trenkler, Christian; Kliebhan, Johannes; Wuertinger, P.; Seger, Christoph; Kaser, Susanne; Mayer, Gert; Pirklbauer, Markus; Ulmer, Hanno; Griesmacher, Andrea

doi:10.1016/s0735-1097(14)60777-4

Cited by 1 publication

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“…High plasma levels of FGF-23 are associated with older age groups (>60 years) (Ix et al, 2012;Kestenbaum et al, 2014;Lutsey et al, 2014;Wright et al, 2014;Masson et al, 2015;Panwar et al, 2015;Speer et al, 2015;Souma et al, 2016;Ter Maaten et al, 2018;Huo et al, 2019), although some studies in younger populations have not found a significant correlation with age (Parker et al, 2010;Agarwal et al, 2014;di Giuseppe et al, 2014;Poelzl et al, 2014;Di Giuseppe et al, 2015;Chonchol et al, 2016;Takahashi et al, 2018). As age increases, metabolic disturbances are more prevalent; therefore, the lack of correlation with age may be due to the lack of metabolic changes.…”

Section: Fgf-23 and Demographic Variables: Age Sex And Ethnicitymentioning

confidence: 99%

“…Interestingly, although the cardiovascular risk is higher in men, elevated FGF-23 levels are more commonly correlated with women (Parker et al, 2010;Seiler et al, 2011;Ix et al, 2012;Agarwal et al, 2014;di Giuseppe et al, 2014;Wright et al, 2014;Di Giuseppe et al, 2015;Masson et al, 2015;Panwar et al, 2015;Speer et al, 2015;Souma et al, 2016;Reindl et al, 2017;Ter Maaten et al, 2018;Cheng et al, 2020) than men (Kestenbaum et al, 2014;Chonchol et al, 2016;Huo et al, 2019). Nevertheless, some authors suggest that levels of FGF-23 could be independent of sex (Shibata et al, 2013;Lutsey et al, 2014;Poelzl et al, 2014;Koller et al, 2015). This discordance could be explained by the fact that most studies were carried out with older patients, including post-menopausal women.…”

Section: Fgf-23 and Demographic Variables: Age Sex And Ethnicitymentioning

confidence: 99%

“…FGF-23 is an early and complementary predictor of adverse cardiac events and could be suitable for improving risk assessment in vulnerable patients with HF or reduced ejection fraction (Koller et al, 2015). FGF-23 is positively correlated with but does not directly depend on the classical biomarkers of cardiac damage, such as N-terminal-pro-B-type natriuretic peptide (NT-proBNP) (Seiler et al, 2011;Shibata et al, 2013;Kestenbaum et al, 2014;Poelzl et al, 2014;Koller et al, 2015;Masson et al, 2015;Panwar et al, 2015;Speer et al, 2015;Wohlfahrt et al, 2015;Ter Maaten et al, 2018;von Jeinsen et al, 2019;Song et al, 2021), high-sensitive cardiac troponin T (hs-cTnT) (Kestenbaum et al, 2014;Masson et al, 2015;Song et al, 2021) and C-reactive protein (CRP) (Parker et al, 2010;Seiler et al, 2011;Ix et al, 2012;Lutsey et al, 2014;Panwar et al, 2015;Speer et al, 2015;Reindl et al, 2017;Song et al, 2021). Furthermore, it has already been demonstrated that the predictive value of the combination of these biomarkers on cardiovascular risk assessment is significantly greater than any of them alone (Wohlfahrt et al, 2015).…”

Section: Fgf-23 and Adverse Cardiac Eventsmentioning

confidence: 99%

“…Age Older > 60 years Lutsey et al, 2014Panwar et al, 2015Masson et al, 2015Ix et al, 2012Wright et al, 2014Kestenbaum et al, 2014Speer et al, 2015Souma et al, 2016Ter Maaten et al, 2018Huo et al, 2019Not Correlated Di Giuseppe et al, 2015di Giuseppe et al, 2014Parker et al, 2010Poelzl et al, 2014Agarwal et al, 2014Chonchol et al, 2016Takahashi et al, 2018Sex Women Di Giuseppe et al, 2015Panwar et al, 2015Masson et al, 2015di Giuseppe et al, 2014Ix et al, 2012Wright et al, 2014Parker et al, 2010Speer et al, 2015Souma et al, 2016Ter Maaten et al, 2018Seiler et al, 2011Reindl et al, 2017Agarwal et al, 2014Cheng et al, 2020Men Kestenbaum et al, 2014Chonchol et al, 2016Huo et al, 2019 Not Correlated Koller et al, 2015Lutsey et al, 2014Shibata et al, 2013Poelzl et al, 2014 Ethnicity Caucasian Ix et al, 2012Chonchol et al, 2016Patel et al, 2020 African American or Hispanic Lutsey et al, 2014…”

Section: Demographic Variablesmentioning

confidence: 99%

“…Nevertheless, the meta-analysis by Marthi et al (2018) did not find a trend across different levels of kidney function in the association between high FGF-23 and HF. From a cardiac functional point of view, many studies have correlated high plasma levels of FGF-23 with a reduced left ventricular ejected fraction (LVEF; <40%), which indicates that high FGF-23 levels are directly linked to systolic dysfunction (Seiler et al, 2011;Shibata et al, 2013;Agarwal et al, 2014;Poelzl et al, 2014;von Jeinsen et al, 2019;Song et al, 2021). Furthermore, high plasma levels of FGF-23 are also associated with albuminuria in CKD which is strongly associated with Heart Failure with reduced Ejection Fraction (HFrEF), but not with Heart Failure with preserved Ejection Fraction (HFpEF) (Nayor et al, 2017).…”

Section: Fgf-23 and Hfmentioning

confidence: 99%

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

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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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