scholarly journals Elevated Serum Fibroblast Growth Factor 21 Is Relevant to Heart Failure Patients with Reduced Ejection Fraction

2022 ◽  
Vol 2022 ◽  
pp. 1-6
Author(s):  
Liuzhang Fan ◽  
Lingyun Gu ◽  
Yuyu Yao ◽  
Genshan Ma
Keyword(s):  
Heart Failure ◽  
Growth Factor ◽  
Ejection Fraction ◽  
Fibroblast Growth Factor ◽  
Left Ventricular ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Reduced Ejection Fraction ◽  
Heart Failure Patients

Objective. The aim of this study was to evaluate the roles of fibroblast growth factor 21 (FGF21) in heart failure patients with reduced ejection fraction and its association with Heart Failure with reduced Ejection Fraction (HFrEF). Methods. The level of FGF21 was measured by enzyme-linked immunosorbent assay (ELISA) in 199 subjects enrolled in this study, including 128 subjects with HFrEF and 71 control subjects. The mean follow-up time was 13.36 months. The left ventricular end-diastolic diameter (LVEDD) and left ventricular ejection fraction (LVEF) percentage were evaluated by the 2D echocardiography. Serum brain natriuretic peptide (BNP) was measured in the routine clinical laboratory. Results. The serum FGF21 level was evidently higher in patients with HFrEF than in the control group ( 228.72 ± 24.04 vs. 171.60 ± 12.98 , p < 0.001 ). After 1 year of follow-up, 61 patients (47.66%) with heart failure were readmitted to the hospital, including 8 deaths (13.11%). The AUC of the receiver operating characteristic (ROC) curve for the predictive value of FGF21 for prognosis was 0.964. Kaplan-Meier analysis results showed that there were significant differences in the 1-year mortality and heart failure readmission events between the grouped subjects. A poor prognosis was correlated with the serum level of FGF21, BNP, LVEDD, and LVEF, which was confirmed by the univariate Cox analysis. Conclusion. FGF21 was independently associated with an increased risk of mortality and readmission HFrEF patients. Therefore, FGF21 has the potential to be a biomarker for the progression of HFrEF in patients.

FGF21 (Fibroblast Growth Factor 21) Defines a Potential Cardiohepatic Signaling Circuit in End-Stage Heart Failure

2021 ◽  
Author(s):  
Salah Sommakia ◽  
Naredos H. Almaw ◽  
Sandra H. Lee ◽  
Dinesh K.A. Ramadurai ◽  
Iosif Taleb ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Growth Factor ◽  
Ejection Fraction ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Reduced Ejection Fraction ◽  
End Stage ◽  
Signaling Circuit

Background: Extrinsic control of cardiomyocyte metabolism is poorly understood in heart failure (HF). FGF21 (Fibroblast growth factor 21), a hormonal regulator of metabolism produced mainly in the liver and adipose tissue, is a prime candidate for such signaling. Methods: To investigate this further, we examined blood and tissue obtained from human subjects with end-stage HF with reduced ejection fraction at the time of left ventricular assist device implantation and correlated serum FGF21 levels with cardiac gene expression, immunohistochemistry, and clinical parameters. Results: Circulating FGF21 levels were substantially elevated in HF with reduced ejection fraction, compared with healthy subjects (HF with reduced ejection fraction: 834.4 [95% CI, 628.4–1040.3] pg/mL, n=40; controls: 146.0 [86.3–205.7] pg/mL, n=20, P =1.9×10 −5 ). There was clear FGF21 staining in diseased cardiomyocytes, and circulating FGF21 levels negatively correlated with the expression of cardiac genes involved in ketone metabolism, consistent with cardiac FGF21 signaling. FGF21 gene expression was very low in failing and nonfailing hearts, suggesting extracardiac production of the circulating hormone. Circulating FGF21 levels were correlated with BNP (B-type natriuretic peptide) and total bilirubin, markers of chronic cardiac and hepatic congestion. Conclusions: Circulating FGF21 levels are elevated in HF with reduced ejection fraction and appear to bind to the heart. The liver is likely the main extracardiac source. This supports a model of hepatic FGF21 communication to diseased cardiomyocytes, defining a potential cardiohepatic signaling circuit in human HF.

scholarly journals Nutraceutical, Dietary, and Lifestyle Options for Prevention and Treatment of Ventricular Hypertrophy and Heart Failure

2021 ◽  
Vol 22 (7) ◽  
pp. 3321
Author(s):  
Mark F. McCarty
Keyword(s):  
Heart Failure ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Ventricular Hypertrophy ◽  
Salt Intake ◽  
Fibroblast Growth Factor 23 ◽  
Research Strategy ◽  
Fibroblast Growth Factor 21 ◽  
High Dose ◽  
Fibroblast Growth

Although well documented drug therapies are available for the management of ventricular hypertrophy (VH) and heart failure (HF), most patients nonetheless experience a downhill course, and further therapeutic measures are needed. Nutraceutical, dietary, and lifestyle measures may have particular merit in this regard, as they are currently available, relatively safe and inexpensive, and can lend themselves to primary prevention as well. A consideration of the pathogenic mechanisms underlying the VH/HF syndrome suggests that measures which control oxidative and endoplasmic reticulum (ER) stress, that support effective nitric oxide and hydrogen sulfide bioactivity, that prevent a reduction in cardiomyocyte pH, and that boost the production of protective hormones, such as fibroblast growth factor 21 (FGF21), while suppressing fibroblast growth factor 23 (FGF23) and marinobufagenin, may have utility for preventing and controlling this syndrome. Agents considered in this essay include phycocyanobilin, N-acetylcysteine, lipoic acid, ferulic acid, zinc, selenium, ubiquinol, astaxanthin, melatonin, tauroursodeoxycholic acid, berberine, citrulline, high-dose folate, cocoa flavanols, hawthorn extract, dietary nitrate, high-dose biotin, soy isoflavones, taurine, carnitine, magnesium orotate, EPA-rich fish oil, glycine, and copper. The potential advantages of whole-food plant-based diets, moderation in salt intake, avoidance of phosphate additives, and regular exercise training and sauna sessions are also discussed. There should be considerable scope for the development of functional foods and supplements which make it more convenient and affordable for patients to consume complementary combinations of the agents discussed here. Research Strategy: Key word searching of PubMed was employed to locate the research papers whose findings are cited in this essay.

scholarly journals Fibroblast Growth Factor 21 and Metabolic Dysfunction in Women with a Prior Glucose-Intolerant Pregnancy

2020 ◽  
Author(s):  
Celeste Durnwald ◽  
Lisa Mele ◽  
Mark B. Landon ◽  
Michael W. Varner ◽  
Brian M. Casey ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 21 ◽  
Prior History ◽  
Metabolic Dysfunction ◽  
Fibroblast Growth ◽  
Index Pregnancy ◽  
History Of

Abstract Objective We sought to determine if there is an association between fibroblast growth factor 21 (FGF21) levels and a history of gestational diabetes mellitus (GDM) in women with and without metabolic dysfunction, defined as a diagnosis of metabolic syndrome or type 2 diabetes (T2DM), 5 to 10 years following participation in a multiple cohort GDM study. Study Design At 5 to 10 years after index pregnancy, women underwent a follow-up visit and were categorized as having no metabolic syndrome, metabolic syndrome, or T2DM. FGF21 levels were compared between women who did and did not have a history of GDM using multivariable linear regression. Results Among 1,889 women, 950 underwent follow-up and 796 had plasma samples analyzed (413 GDM and 383 non-GDM). Total 30.7% of women had been diagnosed with T2DM or metabolic syndrome. Overall, there was no difference in median FGF21 levels in pg/mL between the prior GDM and non-GDM groups (p = 0.12), and the lack of association was observed across all three metabolic categories at follow-up (p for interaction = 0.70). Conclusion There was no association between FGF21 levels and prior history of mild GDM in women with and without metabolic dysfunction 5 to 10 years after the index pregnancy (ClinicalTrials.gov number, NCT00069576, original trial).

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