Fibroblast growth factor-23 and subclinical markers of cardiac dysfunction: The coronary artery risk development in young adults (CARDIA) study

Akhabue, Ehimare; Wong, Mandy; Mehta, Rupal; Isakova, Tamara; Wolf, Myles; Yancy, Clyde W.; Gutiérrez, Orlando M.; Carnethon, Mercedes R.

doi:10.1016/j.ahj.2021.11.009

Cited by 4 publications

(2 citation statements)

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“…Several previous studies have shown an association between high circulating concentrations of FGF23 and a high risk of LVH in the general population (21-24) and patients (25)(26)(27)(28)(29)(30)(31)(32). In addition, there is a particularly strong association in patients with CKD (25,26,28,30,32).…”

Section: Fgf23 and Lvhmentioning

confidence: 91%

Direct and indirect effects of fibroblast growth factor 23 on the heart

2023

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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.

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Section: Fgf23 and Lvhmentioning

confidence: 91%

Direct and indirect effects of fibroblast growth factor 23 on the heart

2023

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“…It is important to note that these toxins are naturally synthesized by the organism, and are essential to preserving mineral balance. Elevated plasmatic FGF-23 causes cardiovascular complications since it can promote cardiac hypertrophy development, and cardiac fibrosis and dysfunction [ 176 , 177 ].…”

Section: Uremic Toxinsmentioning

confidence: 99%

Zebrafish as a Model of Cardiac Pathology and Toxicity: Spotlight on Uremic Toxins

Coppola

Lombari

Mazzella

et al. 2023

IJMS

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Chronic kidney disease (CKD) is an increasing health care problem. About 10% of the general population is affected by CKD, representing the sixth cause of death in the world. Cardiovascular events are the main mortality cause in CKD, with a cardiovascular risk 10 times higher in these patients than the rate observed in healthy subjects. The gradual decline of the kidney leads to the accumulation of uremic solutes with a negative effect on every organ, especially on the cardiovascular system. Mammalian models, sharing structural and functional similarities with humans, have been widely used to study cardiovascular disease mechanisms and test new therapies, but many of them are rather expensive and difficult to manipulate. Over the last few decades, zebrafish has become a powerful non-mammalian model to study alterations associated with human disease. The high conservation of gene function, low cost, small size, rapid growth, and easiness of genetic manipulation are just some of the features of this experimental model. More specifically, embryonic cardiac development and physiological responses to exposure to numerous toxin substances are similar to those observed in mammals, making zebrafish an ideal model to study cardiac development, toxicity, and cardiovascular disease.

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