Fibroblast growth factor 7 alleviates myocardial infarction by improving oxidative stress via PI3Kα/AKT-mediated regulation of Nrf2 and HXK2

Mei, Lin; Chen, Yunjie; Chen, Peng; Chen, Huinan; He, Shengqu; Jin, Cheng; Wang, Yan; Hu, Zhicheng; Li, Wanqian; Jin, Litai; Cong, Weitao; Wang, Xu; Guan, Xueqiang

doi:10.1016/j.redox.2022.102468

Cited by 20 publications

(9 citation statements)

References 74 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The cytoprotective effect of FGF7 has been elucidated to involve the upregulation of NRF2 expression in response to oxidative stress 22,26–28 . The data presented above provides the evidence that FGF7 effectively preserves the functionality of osteoblasts under oxidative stress.…”

Section: Resultsmentioning

confidence: 88%

“…17 Depending on the cell type, FGF7 also has a variety of functions in different physiological processes, such as promoting migration, 18 differentiation, 19 cellcell communication, 20,21 and preventing apoptosis. 22 In particular, FGF7 has exhibited effective cell-protective and regenerative activity in epithelial environments in several in vitro and in vivo experiments. 23,24 Specifically, FGF7 has been clinically used to ameliorate severe oral mucositis caused by cancer chemoradiotherapy.…”

Section: Introductionmentioning

confidence: 99%

“…One possible reason is that FGF7 specifically binds to its receptor, FGFR2IIIb, which is found primarily in epithelial cells 17 . Depending on the cell type, FGF7 also has a variety of functions in different physiological processes, such as promoting migration, 18 differentiation, 19 cell–cell communication, 20,21 and preventing apoptosis 22 . In particular, FGF7 has exhibited effective cell‐protective and regenerative activity in epithelial environments in several in vitro and in vivo experiments 23,24 .…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Fibroblast growth factor 7 protects osteoblasts against oxidative damage through targeting mitochondria

Liu,

Hu,

Niu

et al. 2024

The FASEB Journal

View full text Add to dashboard Cite

The pathophysiology of osteoporosis is significantly influenced by the impaired functioning of osteoblasts, which is particularly caused by oxidative stress. Nevertheless, the underlying mechanisms responsible for this phenomenon are still not well understood. The objective of this study was to elucidate the impact of fibroblast growth factor 7 (FGF7) on the behavior of osteoblasts under conditions of oxidative stress. The osteoblast‐like MC3T3 cells were pretreated with recombinant FGF7 in the presence of oxidative stress induced by hydrogen peroxide (H2O2). We first provided the evidence that the endogenous FGF7 was significantly increased in osteoblasts in response to the increased H2O2 levels. Recombined FGF7 demonstrated a remarkable capacity to resist the detrimental effects of H2O2‐induced oxidative stress, including the increase in cell apoptosis, decrease in osteoblast viability, and impairment in osteogenic differentiation capacity, on osteoblasts. Furthermore, we extensively explored the mechanism underlying these protective effects and discovered a remarkable modulation of reactive oxygen species (ROS) homeostasis in H2O2‐treated cells following the pronounced expression of FGF7, which significantly differed from the control group. Additionally, we observed that FGF7 exerted partial preservation on both the morphology and function of mitochondria when exposed to oxidative stress conditions. Furthermore, FGF7 exhibited the ability to enhance the activation of the p38/MAPK signaling pathway while concurrently suppressing the JNK/MAPK signaling pathway in response to oxidative stress. These results underscore the promising role and underlying mechanisms of FGF7 in preserving osteoblast homeostasis in the face of oxidative stress.

show abstract

Section: Resultsmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Fibroblast growth factor 7 protects osteoblasts against oxidative damage through targeting mitochondria

Liu,

Hu,

Niu

et al. 2024

The FASEB Journal

View full text Add to dashboard Cite

show abstract

“…Beyond our own dataset, we also suggest that this data can be used to identify downstream druggable targets for both study and therapeutic intervention that are not directly implicated in this dataset. This is due to the converging of target miRNAs on several pathways which have been implicated in fibrotic signaling, such as CD47 60 , ITGA2 61, 62 , c-Fos 63, 64 , HXK2 65, 66 , Klotho 67 , p21 68, 69 , and DNMT3a 70 . One particularly interesting connection is that the TGF-β-mediated effects of CD47 and ITGA2 appear downstream of c-Fos, which is known to be involved in AngII-mediated fibrosis 63 and can be regulated by some miRNAs to impact the onset of TGF-β-mediated fibrosis effects 64 in conjunction with AngII-mediated fibrotic signaling around p21 68 .…”

Section: Discussionmentioning

confidence: 99%

Age and Sex-Dependent Differences in Human Cardiac Matrix-Bound Exosomes Modulate Fibrosis through Synergistic miRNA Effects

Ronan

Bahçecioğlu

Yang

et al. 2022

Preprint

View full text Add to dashboard Cite

Aging is a risk factor for cardiovascular disease, the leading cause of death worldwide. Cardiac fibrosis is a harmful result of repeated myocardial infarction that increases risk of morbidity and future injury. Interestingly, rates of cardiac fibrosis are different between young and aged individuals, as well as men and women. Here, for the first time, we identify and isolate matrix-bound extracellular vesicles from the left ventricles (LVs) of young or aged men and women. These LV vesicles (LVVs) show differences in morphology and content between these four cohorts. LVVs effects on fibrosis were also investigated in vitro, and it was shown that aged male LVVs were pro-fibrotic, while other LVVs were anti-fibrotic. miRNAs identified from these LVVs could partially recapitulate these effects together, but not individually, and confer other benefits. These data suggest that synergistic effects of matrix-resident exosomal miRNAs may influence the differential clinical response to MI.

show abstract

“…AAV‐sh‐SPHK1, AAV‐sh‐ATF3, AAV‐oe‐SPHK1, AAV‐sh‐NC, and AAV‐oe‐NC were procured from VectorBuilder. The mice were subjected to anesthesia 1 week after LAD ligation, and AAV were administered into the ischemic heart 18 . The mice were euthanized by sodium pentobarbital at 150 mg/kg ( i.p .)…”

Section: Methodsmentioning

confidence: 99%

ATF3 regulates SPHK1 in cardiomyocyte injury via endoplasmic reticulum stress

Chen,

Luo,

Chen

et al. 2023

Immunity Inflam & Disease

View full text Add to dashboard Cite

AimEndoplasmic reticulum (ER) stress is common in different human pathologies, including cardiac diseases. Sphingosine kinase‐1 (SPHK1) represents an important player in cardiac growth and function. Nevertheless, its function in cardiomyocyte ER stress remains vague. This study sought to evaluate the mechanism through which SPHK1 might influence ER stress during myocardial infarction (MI).MethodsMI‐related GEO data sets were queried to screen differentially expressed genes. Murine HL‐1 cells exposed to oxygen‐glucose deprivation (OGD) and mice with MI were induced, followed by gene expression manipulation using short hairpin RNAs and overexpression vectors. The activating transcription factor 3 (ATF3) and SPHK1 expression was examined in cells and tissues. Cell counting kit‐8, TUNEL, DHE, HE, and Masson's staining were conducted in vitro and in vivo. The inflammatory factor concentrations in mouse serum were measured using ELISA. Finally, the transcriptional regulation of SPHK1 by ATF3 was validated.ResultsATF3 and SPHK1 were upregulated in vivo and in vitro. ATF3 downregulation reduced the SPHK1 transcription. ATF3 and SPHK1 downregulation increased the viability of OGD‐treated HL‐1 cells and decreased apoptosis, oxidative stress, and ER stress. ATF3 and SPHK1 downregulation narrowed the infarction area and attenuated myocardial fibrosis in mice, along with reduced inflammation in the serum and ER stress in the myocardium. In contrast, SPHK1 reduced the protective effect of ATF3 downregulation in vitro and in vivo.ConclusionsATF3 downregulation reduced SPHK1 expression to attenuate cardiomyocyte injury in MI.

show abstract

Fibroblast growth factor 7 alleviates myocardial infarction by improving oxidative stress via PI3Kα/AKT-mediated regulation of Nrf2 and HXK2

Cited by 20 publications

References 74 publications

Fibroblast growth factor 7 protects osteoblasts against oxidative damage through targeting mitochondria

Fibroblast growth factor 7 protects osteoblasts against oxidative damage through targeting mitochondria

Age and Sex-Dependent Differences in Human Cardiac Matrix-Bound Exosomes Modulate Fibrosis through Synergistic miRNA Effects

ATF3 regulates SPHK1 in cardiomyocyte injury via endoplasmic reticulum stress

Contact Info

Product

Resources

About