Fibroblast growth factor 12 attenuated cardiac remodeling via suppressing oxidative stress

Liu, Aijun; Zhang, Yonglin; Xun, Shucan; Zhou, Guangzhi; Lin, Li; Mei, Yong

doi:10.1016/j.peptides.2022.170786

Cited by 7 publications

(6 citation statements)

References 33 publications

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“…Previous study has shown that FGF12 can inhibit cardiac remodeling by inhibiting oxidative stress, indicating its ability to resist myocardial oxidative stress (Liu et al, 2022). Li et al reported that De Novo FGF12 functional variation was potentially associated with idiopathic ventricular tachycardia (Li et al, 2017).…”

Section: Discussionmentioning

confidence: 98%

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FGF12 restrains mitochondria‐dependent ferroptosis in doxorubicin‐induced cardiomyocytes through the activation of FGFR1/AMPK/NRF2 signaling

Tian,

Li,

Wang

et al. 2024

Drug Development Research

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Fibroblast growth factor‐12 (FGF12) has been reported to play important role in regulating heart diseases. We aimed to explore the role of FGF12 in doxorubicin (DOX)‐induced myocardial injury. DOX‐induced mice and DOX‐induced HL‐1 cells were used as the myocardial injury in vivo and in vitro. Then, FGF12, Anp, Bnp, and Myh7 expression was detected. The pathological injury in myocardium tissue was observed by H&E staining. The levels of markers related to myocardial damage and oxidative stress were assessed. Then, immunohistochemistry and immunofluorescence staining were used to detect FGF12 and 4‐HNE expression. Ferroptosis were detected by Prussian blue staining and western blot. The FGFR1/AMPK/NRF2 signaling was measured by western blot. FGF12 expression was downregulated in DOX‐induced mice myocardium tissues. FGF12 overexpression alleviated DOX‐induced myocardial tissue pathological injury and reduced Anp, Bnp, and Myh7 expression. Additionally, the levels of CK‐MB, LDH and cTnT in serum were decreased after FGF12 upregulation in DOX‐induced mice. Moreover, FGF12 overexpression reduced the levels of ROS, MDA, and 4‐HNE but increased SOD and GSH‐Px activities. Meanwhile, FGF12 led to less deposition of iron ion, decreased ACSL4, PTGS2 and increased GPX4, FTH1 expression. Additionally, FGF12 activated the expressions of FGFR1, p‐AMPK, and NRF2. Moreover, FGFR1 silencing reversed the protective effects of FGF12 overexpression on cell viability, oxidative stress, ferroptosis, and FGFR1/AMPK/NRF2 pathway. To sum up, FGF12 inhibited mitochondria‐dependent ferroptosis in cardiomyocytes induced by DOX through activation of FGFR1/AMPK/NRF2 signaling. These findings clarify a new mechanism of DOX‐induced cardiac injury and provide a promising target to limit the disease development.

show abstract

Section: Discussionmentioning

confidence: 98%

“…Previous study has shown that FGF12 can inhibit cardiac remodeling by inhibiting oxidative stress, indicating its ability to resist myocardial oxidative stress (Liu et al, 2022). Li et al…”

Section: Discussionmentioning

confidence: 99%

FGF12 restrains mitochondria‐dependent ferroptosis in doxorubicin‐induced cardiomyocytes through the activation of FGFR1/AMPK/NRF2 signaling

Tian,

Li,

Wang

et al. 2024

Drug Development Research

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“…Although little is known about the expression or role of FGF12 in the ovary, reports indicate that FGF12 is highly expressed in the nervous system and positively regulates voltage-gated sodium channels in neurons [81]. Recent studies also revealed that FGF12 is expressed in the heart and vascular smooth muscle cells, and lower FGF12 is associated with vascular wall thickening in atherosclerosis and pulmonary arterial hypertension [82][83][84]. Our studies also showed that PGF2α injection slightly elevated and then reduced the expression of FGF7 mRNA.…”

Section: Discussionmentioning

confidence: 99%

Basic fibroblast growth factor induces proliferation and collagen production by fibroblasts derived from the bovine corpus luteum

Monaco

Plewes

Przygrodzka

et al. 2023

Biology of Reproduction

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Cyclic regression of the ovarian corpus luteum, the endocrine gland responsible for progesterone production, involves rapid matrix remodeling. Despite fibroblasts in other systems being known for producing and maintaining extracellular matrix, little is known about fibroblasts in the functional or regressing corpus luteum. Vast transcriptomic changes occur in the regressing corpus luteum, among which are reduced levels of vascular endothelial growth factor a (VEGFA) and increased expression of fibroblast growth factor 2 (FGF2) after 4 and 12 h of induced regression, when progesterone is declining, and the microvasculature is destabilizing. We hypothesized that FGF2 activates luteal fibroblasts. Analysis of transcriptomic changes during induced luteal regression revealed elevations in markers of fibroblast activation and fibrosis, including fibroblast activation protein (FAP), serpin family E member 1 (SERPINE1), and secreted phosphoprotein 1 (SPP1). To test our hypothesis, we treated bovine luteal fibroblasts with FGF2 to measure downstream signaling, type 1 collagen production, and proliferation. We observed rapid and robust phosphorylation of various signaling pathways involved in proliferation, such as ERK, AKT, and STAT1. From our longer-term treatments, we determined that FGF2 has a concentration-dependent collagen-inducing effect, and that FGF2 acts as a mitogen for luteal fibroblasts. FGF2-induced proliferation was greatly blunted by inhibition of AKT or STAT1 signaling. Our results suggest that luteal fibroblasts are responsive to factors that are released by the regressing bovine corpus luteum, an insight into the contribution of fibroblasts to the microenvironment in the regressing corpus luteum.

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“…The role of FGF-12 is mainly investigated in cardiovascular disease. FGF-12 upregulation can improve cardiac dysfunction in mice with myocardial infarction by reducing the production of extracellular matrix components in cardiac fibroblasts induced by angiotensin II, including fibronectin and collagens I and III[ 53 ]. It also plays an important role in vascular remodeling by regulating the phenotypic change of vascular smooth muscle cells[ 54 ].…”

Section: Fgfs Play An Important Role In Diabetes and Related Diseasesmentioning

confidence: 99%

Roles of fibroblast growth factors in the treatment of diabetes

Zhang,

Yang

2024

World J Diabetes

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Diabetes affects about 422 million people worldwide, causing 1.5 million deaths each year. However, the incidence of diabetes is increasing, including several types of diabetes. Type 1 diabetes (5%-10% of diabetic cases) and type 2 diabetes (90%-95% of diabetic cases) are the main types of diabetes in the clinic. Accumulating evidence shows that the fibroblast growth factor (FGF) family plays important roles in many metabolic disorders, including type 1 and type 2 diabetes. FGF consists of 23 family members (FGF-1-23) in humans. Here, we review current findings of FGFs in the treatment of diabetes and management of diabetic complications. Some FGFs (e.g., FGF-15, FGF-19, and FGF-21) have been broadly investigated in preclinical studies for the diagnosis and treatment of diabetes, and their therapeutic roles in diabetes are currently under investigation in clinical trials. Overall, the roles of FGFs in diabetes and diabetic complications are involved in numerous processes. First, FGF intervention can prevent high-fat diet-induced obesity and insulin resistance and reduce the levels of fasting blood glucose and triglycerides by regulating lipolysis in adipose tissues and hepatic glucose production. Second, modulation of FGF expression can inhibit renal and cardiac fibrosis by regulating the expression of extracellular matrix components, promote diabetic wound healing process and bone repair, and inhibit cancer cell proliferation and migration. Finally, FGFs can regulate the activation of glucose-excited neurons and the expression of thermogenic genes.

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Fibroblast growth factor 12 attenuated cardiac remodeling via suppressing oxidative stress

Cited by 7 publications

References 33 publications

FGF12 restrains mitochondria‐dependent ferroptosis in doxorubicin‐induced cardiomyocytes through the activation of FGFR1/AMPK/NRF2 signaling

FGF12 restrains mitochondria‐dependent ferroptosis in doxorubicin‐induced cardiomyocytes through the activation of FGFR1/AMPK/NRF2 signaling

Basic fibroblast growth factor induces proliferation and collagen production by fibroblasts derived from the bovine corpus luteum

Roles of fibroblast growth factors in the treatment of diabetes

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