Fibroblast growth factor 21 in heart failure

Tucker, William; Tucker, Bradley; Rye, Kerry‐Anne

doi:10.1007/s10741-022-10268-0

Cited by 20 publications

(13 citation statements)

References 114 publications

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“…Tucker et al [ 19 ] concluded in their review study, which summarized preclinical and clinical evidence, that FGF21 plays a function in HF. Preclinical studies have demonstrated that FGF21 has a role in the development of heart failure by mitigating oxidative stress, cardiac hypertrophy, and inflammation in cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

The Correlation Between Serum Fibroblast Growth Factor 21 and the Severity and Occurrence of Coronary Artery Disease

Sinha,

Prakash,

Keshari

et al. 2024

Cureus

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Background: The burden of cardiovascular diseases (CVDs) is increasing worldwide with CVD being one of the leading causes of death, including atherosclerosis, myocardial infarction, cardiomyopathy, and heart failure (HF). Fibroblast growth factor 21 (FGF21) is an endocrine hormone that regulates carbohydrate and lipid metabolism. It exerts direct effects on the cardiovascular system and can serve as an early indicator of CVDs. FGF21's therapeutic properties include reducing obesity, dyslipidaemia, and hyperglycemia, which can help treat metabolic disorders, autophagy, and apoptosis. Atherosclerosis is developed due to chronic inflammatory conditions, and the immune system's reaction to oxidized lipoproteins is mainly responsible for the development of atherosclerosis. FGF21's precise role in the pathogenesis of coronary artery disease (CAD) remains elusive. Aim: This study aimed to assess the role of FGF21 in predicting the severity and magnitude of CAD in individuals diagnosed with stable angina pectoris (SAP). Materials and methods: A prospective cross-sectional study was conducted on 110 consecutive patients with SAP reported to the cardiology department of the Indira Gandhi Institute of Medical Sciences (IGIMS), Patna, India. They were divided into two groups based on coronary angiography findings. Control groups included patients not showing any atherosclerotic lesions and case groups with atherosclerotic lesions. The SYNTAX score is a grading system that measures the location and complexity of coronary arteries using anatomical principles. The Gensini score assessment technique was employed to determine the severity of CAD. We compared serum FGF21 levels,left ventricular ejection fraction (LVEF), and inflammatory biomarker C-reactive protein (CRP) levels between the two groups. Moreover, we examined the correlation between the serum FGF21 level and the SYNTAX and Gensini scores. The statistical analysis was done using Version 23.0 of SPSS Statistics. P-values below 0.05 were considered statistically significant. Results: The study found that the case group had a higher average age and a higher proportion of male patients. The case group had considerably higher levels of FGF21 (166.59 ± 94.49791 pg/mL) compared to the control group (54.13 ± 48.467 pg/mL) (p=0.034). The LVEF exhibited a significant difference between the case and control groups, with mean values of 50.3056 ± 7.8242% and 56.078 ± 5.3987%, respectively (p=0.031). CRP levels were comparable in both groups. The case group had mean values of SYNTAX and Gensini scores of 23.19±7.43 and 50.03±27.30, respectively. We found that there was no statistically significant association between the risk assessments for CAD severity and the levels of serum FGF21 (correlation coefficient r=0.14070, p>0.05, and r=0.206415, p>0.05, respectively) Conclusions: FGF21 is gaining recognition as a prospective addition to the FGF family, potentially playing a significant role in cardiovascular disease, particularly ather...

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Section: Discussionmentioning

confidence: 99%

The Correlation Between Serum Fibroblast Growth Factor 21 and the Severity and Occurrence of Coronary Artery Disease

Sinha,

Prakash,

Keshari

et al. 2024

Cureus

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“… 41 FGF‐21 has also been implicated in the pathogenesis of HF through the modulation of oxidative stress. 42 Tucker et al 43 reported that FGF‐21 is involved in the pathophysiology of HF by preventing oxidative stress, cardiac hypertrophy, and inflammation in cardiomyocytes and that its level is elevated in patients with HF, suggesting that FGF‐21 may be used as a biomarker for the prediction and diagnosis of HF. Another study found that the serum FGF21 levels were elevated in hospitalized patients with ST‐segment elevation myocardial infarction (STEMI), confirming that elevated serum FGF‐21 level may be a strong predictor of HF during hospitalization in patients with STEMI.…”

Section: Discussionmentioning

confidence: 99%

Role of serum cytokines in the prediction of heart failure in patients with coronary artery disease

Hou,

Sun,

Zhao

et al. 2023

ESC Heart Failure

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AimsCoronary artery disease (CAD) is the most common cause of heart failure (HF). This study aimed to identify cytokine biomarkers for predicting HF in patients with CAD.Methods and resultsTwelve patients with CAD without HF (CAD‐non HF), 12 patients with CAD complicated with HF (CAD‐HF), and 12 healthy controls were enrolled for Human Cytokine Antibody Array, which were used as the training dataset. Then, differentially expressed cytokines among the different groups were identified, and crucial characteristic proteins related to CAD‐HF were screened using a combination of the least absolute shrinkage and selection operator, recursive feature elimination, and random forest methods. A support vector machine (SVM) diagnostic model was constructed based on crucial characteristic proteins, followed by receiver operating characteristic curve analysis. Finally, two validation datasets, GSE20681 and GSE59867, were downloaded to verify the diagnostic performance of the SVM model and expression of crucial proteins, as well as enzyme‐linked immunosorbent assay was also used to verify the levels of crucial proteins in blood samples. In total, 12 differentially expressed proteins were overlapped in the three comparison groups, and then four optimal characteristic proteins were identified, including VEGFR2, FLRG, IL‐23, and FGF‐21. After that, the area under the receiver operating characteristic curve of the constructed SVM classification model for the training dataset was 0.944. The accuracy of the SVM classification model was validated using the GSE20681 and GSE59867 datasets, with area under the receiver operating characteristic curve values of 0.773 and 0.745, respectively. The expression trends of the four crucial proteins in the training dataset were consistent with those in the validation dataset and those determined by enzyme‐linked immunosorbent assay.ConclusionsThe combination of VEGFR2, FLRG, IL‐23, and FGF‐21 can be used as a candidate biomarker for the prediction and prevention of HF in patients with CAD.

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“…The impact of in ammation extends to FGF-mediated cell survival pathways, as in ammatory signals may modulate these pathways, potentially compromising the anti-apoptotic effects of FGF and in uencing overall cardiomyocyte survival. FGF signaling's involvement in angiogenesis and its promotion of cardiomyocyte proliferation during development may be negatively affected by in ammation, potentially leading to impaired vascularization and a reduction in the expansion of the cardiomyocyte population [140,141]. The intricate crosstalk between FGF signaling and other pathways, such as Wnt and Notch, is also susceptible to disruption by in ammation, potentially compromising the integrated signaling network that regulates cardiac cell fate.…”

Section: Fgf Signaling Pathwaymentioning

confidence: 99%

Investigating the Development and Progression of Myocarditis through the lens of the Genetic Architecture of Cardiomyocytes

Shafi,

Khan,

Virk

2024

Preprint

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Background: Myocarditis-induced inflammation disrupts the intricate genetic architecture governing cardiomyocyte development and function. Understanding the specific disruptions in key regulators, such as Isl1, Nkx2–5, GATA4, and signaling pathways like Wnt and BMPs, is crucial for unraveling the molecular underpinnings of cardiac dysfunction. This investigation holds paramount importance in informing targeted therapeutic strategies to mitigate inflammation-induced genetic disruptions, offering potential breakthroughs in the management of myocarditis and improving outcomes for affected individuals. Methods: Databases, including PubMed, MEDLINE, and Google Scholar, were searched for published articles without any date restrictions, focusing on cardiac genes, signaling pathways, and transcription factors, with an emphasis on NF-κB in myocarditis. This study adheres to relevant PRISMA guidelines (Preferred Reporting Items for Systematic Reviews and Meta-Analyses). Results: This study reveals profound disruptions in the genetic architecture of cardiomyocytes. Transcriptional regulatory networks crucial for cardiomyocyte differentiation, including Isl1, Nkx2–5, GATA4, and Tbx5, exhibit altered expression patterns, suggesting compromised maturation processes. The Brg1/Baf60 – Smarcd3 complex, HAND1/2, and MYOCD, essential for cardiogenic regulation, are susceptible to inflammatory damage, impacting cell fate determination. NF-κB-mediated damage to BMPs and the Wnt-signaling pathway results in downstream shifts, affecting gene expression dynamics. These disruptions, coupled with compromised survival mechanisms and heightened apoptotic susceptibility, contribute to cardiac dysfunction and increased arrhythmogenic risk. Altered ECM remodeling and fibrosis further underscore the complexity of myocarditis-induced genetic alterations. Insights from these results hold implications for developing targeted therapeutic strategies aimed at mitigating inflammation-induced genetic disruptions and preserving cardiac health in the context of myocarditis. Conclusion: Myocarditis-induced inflammation disrupts the intricate genetic architecture of cardiomyocytes, compromising key regulators like Isl1, Brg1/Baf60 complex, Nkx2–5, GATA4, Tbx5, Mef2c, HAND1/2, MYOCD, MSX2, HOPX, Wnt signaling, Notch, FGF, and BMPs. This disruption leads to impaired cardiomyocyte differentiation, compromised survival mechanisms, dysregulated ECM remodeling, and heightened pro-inflammatory responses, collectively resulting in cardiac dysfunction and structural abnormalities. Targeted therapeutic interventions to mitigate inflammation-induced genetic disruptions are crucial for preserving optimal cardiac function in the challenging landscape of myocarditis.

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Fibroblast growth factor 21 in heart failure

Cited by 20 publications

References 114 publications

The Correlation Between Serum Fibroblast Growth Factor 21 and the Severity and Occurrence of Coronary Artery Disease

The Correlation Between Serum Fibroblast Growth Factor 21 and the Severity and Occurrence of Coronary Artery Disease

Role of serum cytokines in the prediction of heart failure in patients with coronary artery disease

Investigating the Development and Progression of Myocarditis through the lens of the Genetic Architecture of Cardiomyocytes

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