Regulatory role of endogenous and exogenous fibroblast growth factor 1 in the cardiovascular system and related diseases

Xiao, Mengjie; Tang, Yufeng; A, Jie Wang; B, Jie Wang; Lu, Guangping; Guo, Yuanfang; Zhang, Jingjing; Gu, Junlian

doi:10.1016/j.phrs.2021.105596

Cited by 5 publications

(6 citation statements)

References 93 publications

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“…Our study and other previous studies have verified that FGF1, as a powerful metabolic hormone, played a pivotal role in diabetic complication and displayed the favorable effects on maintaining myocardial integrity and protecting against cardiac dysfunction in response to DOX [ 8 , 32 , 33 , 34 , 35 ]. Therefore, FGF1 has a great prospect of clinical application in cardiovascular disease.…”

Section: Discussionsupporting

confidence: 82%

“…Multiple works identified that fibroblast growth factor 1 (FGF1) is elevated by oxidative damage, implying that an increased FGF1 expression is an adaptive response and might be protective under different kinds of stresses. Our previous study revealed that FGF1 displayed therapeutics and favorable effects on maintaining myocardial redox homeostasis and improving cardiac function, especially in the setting of DOX treatment [ 8 , 9 ]. Beyond that, FGF1 is now emerging as possessing various protective effects including but not restricted to promoting angiogenesis [ 10 ] and alleviating apoptosis [ 11 ] and fibrosis [ 9 ] through partly attenuating oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

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Resveratrol and FGF1 Synergistically Ameliorates Doxorubicin-Induced Cardiotoxicity via Activation of SIRT1-NRF2 Pathway

Liu

Gao

et al. 2022

Nutrients

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Doxorubicin (DOX) has received attention due to dose-dependent cardiotoxicity through abnormal redox cycling. Native fibroblast growth factor 1 (FGF1) is known for its anti-oxidative benefits in cardiovascular diseases, but possesses a potential tumorigenic risk. Coincidentally, the anti-proliferative properties of resveratrol (RES) have attracted attention as alternatives or auxiliary therapy when combined with other chemotherapeutic drugs. Therefore, the purpose of this study is to explore the therapeutic potential and underlying mechanisms of co-treatment of RES and FGF1 in a DOX-treated model. Here, various cancer cells were applied to determine whether RES could antagonize the oncogenesis effect of FGF1. In addition, C57BL/6J mice and H9c2 cells were used to testify the therapeutic potential of a co-treatment of RES and FGF1 against DOX-induced cardiotoxicity. We found RES could reduce the growth-promoting activity of FGF1. Additionally, the co-treatment of RES and FGF1 exhibits a more powerful cardio-antioxidative capacity in a DOX-treated model. The inhibition of SIRT1/NRF2 abolished RES in combination with FGF1 on cardioprotective action. Further mechanism analysis demonstrated that SIRT1 and NRF2 might form a positive feedback loop to perform the protective effect on DOX-induced cardiotoxicity. These favorable anti-oxidative activities and reduced proliferative properties of the co-treatment of RES and FGF1 provided a promising therapy for anthracycline cardiotoxicity during chemotherapy.

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Section: Discussionsupporting

confidence: 82%

Section: Introductionmentioning

confidence: 99%

Resveratrol and FGF1 Synergistically Ameliorates Doxorubicin-Induced Cardiotoxicity via Activation of SIRT1-NRF2 Pathway

Liu

Gao

et al. 2022

Nutrients

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“…FGF1 was first identified as a classical mitogen, as such, most early exploration of its therapeutic applications focused on angiogenesis, cardio protection, nerve and skeletal muscle regeneration, and wound healing, banking on its prosurvival and proliferative effects. [37][38][39] The discovery of metabolic regulatory activity of FGF1 has broaden its functional diversity and generated new hope for metabolic disease therapies such as for MAFLD and T2D. [8][9][10] However, the classical signaling pathways, such as the PLCγ/PKC, FRS2α/RAS-MAPK and Gab1/PI3 kinase/Akt and CrkL/Cdc42-Rac [40][41][42][43] underlie the mitogenic activity of most paracrine FGFs, can hardly explain the potent and distinct metabolic regulatory activities of FGF1.…”

Section: Discussionmentioning

confidence: 99%

FGF1 ameliorates obesity‐associated hepatic steatosis by reversing IGFBP2 hypermethylation

et al. 2023

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Obesity is a major contributing factor for metabolic-associated fatty liver disease (MAFLD). Fibroblast growth factor (FGF) 1 is the first paracrine FGF family member identified to exhibit promising metabolic regulatory properties capable of conferring glucose-lowering and insulin-sensitizing effect. This study explores the role and molecular underpinnings of FGF1 in obesity-associated hepatic steatosis. In a mouse high-fat diet (HFD)-induced MAFLD model, chronic treatment with recombinant FGF1(rFGF1) was found to effectively reduce the severity of insulin resistance, hyperlipidemia, and inflammation. FGF1 treatment decreased lipid accumulation in the mouse liver and palmitic acid-treated AML12 cells. These effects were associated with decreased mature form SREBF1 expression and its target genes FASN and SCD1. Interestingly, we uncovered that rFGF1 significantly induced IGFBP2 expression at both mRNA and protein levels in HFD-fed mouse livers and cultured hepatocytes treated with palmitic acid.Adeno-associated virus-mediated IGFBP2 suppression significantly diminished the therapeutic benefit of rFGF1 on MAFLD-associated phenotypes, indicating that IGFBP2 plays a crucial role in the FGF1-mediated reduction of hepatic steatosis. Further analysis revealed that rFGF1 treatment reduces the recruitment of DNA methyltransferase 3 alpha to the IGFBP2 genomic locus, leading to decreased IGFBP2 gene methylation and increased mRNA and protein expression.Collectively, our findings reveal FGF1 modulation of lipid metabolism via epigenetic regulation of IGFBP2 expression, and unravel the therapeutic potential of the FGF1-IGFBP2 axis in metabolic diseases associated with obesity.

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“…Moreover, fibroblast growth factor-1 (FGF-1) belongs to the FGF family and has been shown to inhibit fibroblast collagen production and differentiation into myofibroblasts, and reverse the epithelial-mesenchymal transition by inhibiting TGF-β1 signaling pathways (Gasser et al, 2022). FGF-1 participates in many vital functions in the cell, such as the axial structuring of embryonic tissues, identification and differentiation of cell types, morphogenesis of organs and systems such as the vascular system, and regulation of cell proliferation and movement (Xiao et al, 2021). In addition, it has a role in many biological events from tissue repair to cancer cell growth and spread (Coleman et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Protective effects of resveratrol on permethrin-induced fetotoxicity in rats

YÜKSEL¹,

ASLAN

Tosun

et al. 2023

Anatolian Journal of Botany

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Synthetic pyrethroid insecticides have been widely used for years to be protected from the harmful effects of insects and control disease vectors. In this study, the potential effects of resveratrol, a polyphenolic compound, against the potential toxicity of permethrin, an effective pyrethroid derivative, on the fetus were investigated. In the study, Wistar female rats were divided into four groups Control, Sham, Permethrin, and Permethrin + Resveratrol. The lung, liver, kidney, and small intestine development of fetuses were evaluated histopathologically. Also, Bone Morphogenetic Protein 4 (BMP-4) in bone tissue development and Fibroblast Growth Factor-1 (FGF-1) expressions in the lung were examined immunohistochemically. All structures in the control and sham groups were normal. Permethrin caused epithelial damage, regression in bronchial and primitive alveolar development in the lung; congestion, edema, and sinusoidal dilatation around the central vein in the liver; tubular epithelial degeneration, regression in glomeruli and tubule formation in the kidney; epithelial degeneration and irregularity in the villus structure in the small intestine. Immunohistochemical results indicated that permethrin administration decreased BMP-4 levels in bone tissue and FGF-1 levels in the lung. After resveratrol application was found to greatly alleviate histopathological and immunohistopathological variability in all tissues. Oral consumption of permethrin by pregnant rats caused growth retardation and tissue damage in many different tissues in offspring. Intake of resveratrol during pregnancy showed protective effects against fetotoxicity caused by permethrin.

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Regulatory role of endogenous and exogenous fibroblast growth factor 1 in the cardiovascular system and related diseases

Cited by 5 publications

References 93 publications

Resveratrol and FGF1 Synergistically Ameliorates Doxorubicin-Induced Cardiotoxicity via Activation of SIRT1-NRF2 Pathway

Resveratrol and FGF1 Synergistically Ameliorates Doxorubicin-Induced Cardiotoxicity via Activation of SIRT1-NRF2 Pathway

FGF1 ameliorates obesity‐associated hepatic steatosis by reversing IGFBP2 hypermethylation

Protective effects of resveratrol on permethrin-induced fetotoxicity in rats

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