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  1. AU="He, Shengqu"
  2. AU="Elec, Florin I"
  3. AU="I.S. Carneiro"
  4. AU="Jia, Dongzheng" AU="Jia, Dongzheng"
  5. AU="Hollis-Perry, Monique"
  6. AU="Duman, Duygu"
  7. AU="Abdullahi, Akilu"
  8. AU="Daniela Maymó"

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  1. Artikel ; Online: Metformin alleviates ethanol-induced cardiomyocyte injury by activating AKT/Nrf2 signaling in an ErbB2-dependent manner

    Chen, Yunjie / Zhu, Suyan / Lin, Zhu / Zhang, Yuanbin / Jin, Cheng / He, Shengqu / Chen, Xueqin / Zhou, Xuan

    Mol Biol Rep. 2023 Apr., v. 50, no. 4 p.3469-3478

    2023  

    Abstract: BACKGROUND: Metformin, a first-line oral anti-diabetic drug, has recently been reported to exert protective effect on various cardiovascular diseases. However, the potential role of metformin in ethanol-induced cardiomyocyte injury is still unknown. ... ...

    Abstract BACKGROUND: Metformin, a first-line oral anti-diabetic drug, has recently been reported to exert protective effect on various cardiovascular diseases. However, the potential role of metformin in ethanol-induced cardiomyocyte injury is still unknown. Therefore, this study was aimed to investigate the effect of metformin on ethanol-induced cardiomyocyte injury and its underlying mechanism. METHODS AND RESULTS: H9c2 cardiomyocytes were exposed to ethanol for 24 h to establish an ethanol-induced cardiomyocyte injury model, and followed by treatment with metformin in the presence or absence of Lapatinib (an ErbB2 inhibition). CCK8 and LDH assays demonstrated that metformin improved cell viability in cardiomyocytes exposed to ethanol. Furthermore, metformin suppressed cardiomyocyte apoptosis and reduced the expressions of apoptosis-related proteins (Bax and C-CAS-3). In addition, our results showed that metformin activated the AKT/Nrf2 pathway, and then promoted Nrf2 nuclear translocation and the transcription of its downstream antioxidant genes (HO-1, CAT and SOD2), thereby inhibiting oxidative stress. Interestingly, we found that ErbB2 protein expression was significantly inhibited in ethanol-treated cardiomyocytes, which was markedly reversed by metformin. In contrast, Lapatinib largely abrogated the activation of AKT/Nrf2 signaling by metformin, accompanied by the increases in oxidative stress and cardiomyocyte apoptosis, indicating that metformin prevented ethanol-induced cardiomyocyte injury in an ErbB2-dependent manner. CONCLUSION: In summary, our study provides the first evidence that metformin protects cardiomyocyte against ethanol-induced oxidative stress and apoptosis by activating ErbB2-mediated AKT/Nrf2 signaling. Thus, metformin may be a potential novel treatment approach for alcoholic cardiomyopathy.
    Schlagwörter antioxidants ; apoptosis ; cardiomyocytes ; cardiomyopathy ; cell viability ; ethanol ; metformin ; models ; oxidative stress ; protective effect ; protein synthesis
    Sprache Englisch
    Erscheinungsverlauf 2023-04
    Umfang p. 3469-3478.
    Erscheinungsort Springer Netherlands
    Dokumenttyp Artikel ; Online
    ZDB-ID 186544-4
    ISSN 1573-4978 ; 0301-4851
    ISSN (online) 1573-4978
    ISSN 0301-4851
    DOI 10.1007/s11033-023-08310-x
    Datenquelle NAL Katalog (AGRICOLA)

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    Verfügbar in ZB MED Bonn

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  2. Artikel ; Online: Metformin alleviates ethanol-induced cardiomyocyte injury by activating AKT/Nrf2 signaling in an ErbB2-dependent manner.

    Chen, Yunjie / Zhu, Suyan / Lin, Zhu / Zhang, Yuanbin / Jin, Cheng / He, Shengqu / Chen, Xueqin / Zhou, Xuan

    Molecular biology reports

    2023  Band 50, Heft 4, Seite(n) 3469–3478

    Abstract: Background: Metformin, a first-line oral anti-diabetic drug, has recently been reported to exert protective effect on various cardiovascular diseases. However, the potential role of metformin in ethanol-induced cardiomyocyte injury is still unknown. ... ...

    Abstract Background: Metformin, a first-line oral anti-diabetic drug, has recently been reported to exert protective effect on various cardiovascular diseases. However, the potential role of metformin in ethanol-induced cardiomyocyte injury is still unknown. Therefore, this study was aimed to investigate the effect of metformin on ethanol-induced cardiomyocyte injury and its underlying mechanism.
    Methods and results: H9c2 cardiomyocytes were exposed to ethanol for 24 h to establish an ethanol-induced cardiomyocyte injury model, and followed by treatment with metformin in the presence or absence of Lapatinib (an ErbB2 inhibition). CCK8 and LDH assays demonstrated that metformin improved cell viability in cardiomyocytes exposed to ethanol. Furthermore, metformin suppressed cardiomyocyte apoptosis and reduced the expressions of apoptosis-related proteins (Bax and C-CAS-3). In addition, our results showed that metformin activated the AKT/Nrf2 pathway, and then promoted Nrf2 nuclear translocation and the transcription of its downstream antioxidant genes (HO-1, CAT and SOD2), thereby inhibiting oxidative stress. Interestingly, we found that ErbB2 protein expression was significantly inhibited in ethanol-treated cardiomyocytes, which was markedly reversed by metformin. In contrast, Lapatinib largely abrogated the activation of AKT/Nrf2 signaling by metformin, accompanied by the increases in oxidative stress and cardiomyocyte apoptosis, indicating that metformin prevented ethanol-induced cardiomyocyte injury in an ErbB2-dependent manner.
    Conclusion: In summary, our study provides the first evidence that metformin protects cardiomyocyte against ethanol-induced oxidative stress and apoptosis by activating ErbB2-mediated AKT/Nrf2 signaling. Thus, metformin may be a potential novel treatment approach for alcoholic cardiomyopathy.
    Mesh-Begriff(e) Apoptosis ; Cell Line ; Ethanol/pharmacology ; Lapatinib/pharmacology ; Metformin/pharmacology ; Metformin/metabolism ; Myocytes, Cardiac/metabolism ; NF-E2-Related Factor 2/metabolism ; Oxidative Stress ; Proto-Oncogene Proteins c-akt/metabolism ; Receptor, ErbB-2/metabolism
    Chemische Substanzen Ethanol (3K9958V90M) ; Lapatinib (0VUA21238F) ; Metformin (9100L32L2N) ; NF-E2-Related Factor 2 ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Receptor, ErbB-2 (EC 2.7.10.1)
    Sprache Englisch
    Erscheinungsdatum 2023-02-11
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article
    ZDB-ID 186544-4
    ISSN 1573-4978 ; 0301-4851
    ISSN (online) 1573-4978
    ISSN 0301-4851
    DOI 10.1007/s11033-023-08310-x
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: 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, Yang / Hu, Zhicheng / Li, Wanqian / Jin, Litai / Cong, Weitao / Wang, Xu / Guan, Xueqiang

    Redox biology

    2022  Band 56, Seite(n) 102468

    Abstract: Acute myocardial infarction (MI) triggers oxidative stress, which worsen cardiac function, eventually leads to remodeling and heart failure. Unfortunately, effective therapeutic approaches are lacking. Fibroblast growth factor 7 (FGF7) is proved with ... ...

    Abstract Acute myocardial infarction (MI) triggers oxidative stress, which worsen cardiac function, eventually leads to remodeling and heart failure. Unfortunately, effective therapeutic approaches are lacking. Fibroblast growth factor 7 (FGF7) is proved with respect to its proliferative effects and high expression level during embryonic heart development. However, the regulatory role of FGF7 in cardiovascular disease, especially MI, remains unclear. FGF7 expression was significantly decreased in a mouse model at 7 days after MI. Further experiments suggested that FGF7 alleviated MI-induced cell apoptosis and improved cardiac function. Mechanistic studies revealed that FGF7 attenuated MI by inhibiting oxidative stress. Overexpression of FGF7 actives nuclear factor erythroid 2-related factor 2 (Nrf2) and scavenging of reactive oxygen species (ROS), and thereby improved oxidative stress, mainly controlled by the phosphatidylinositol-3-kinase α (PI3Kα)/AKT signaling pathway. The effects of FGF7 were partly abrogated in Nrf2 deficiency mice. In addition, overexpression of FGF7 promoted hexokinase2 (HXK2) and mitochondrial membrane translocation and suppressed mitochondrial superoxide production to decrease oxidative stress. The role of HXK2 in FGF7-mediated improvement of mitochondrial superoxide production and protection against MI was verified using a HXK2 inhibitor (3-BrPA) and a HXKII VDAC binding domain (HXK2VBD) peptide, which competitively inhibits localization of HXK2 on mitochondria. Furthermore, inhibition of PI3Kα/AKT signaling abolished regulation of Nrf2 and HXK2 by FGF7 upon MI. Together, these results indicate that the cardio protection of FGF7 under MI injury is mostly attributable to its role in maintaining redox homeostasis via Nrf2 and HXK2, which is mediated by PI3Kα/AKT signaling.
    Mesh-Begriff(e) Animals ; Fibroblast Growth Factor 7/metabolism ; Fibroblast Growth Factor 7/pharmacology ; Mice ; Myocardial Infarction/genetics ; Myocardial Infarction/metabolism ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Oxidative Stress ; Phosphatidylinositol 3-Kinase/metabolism ; Phosphatidylinositols/pharmacology ; Proto-Oncogene Proteins c-akt/metabolism ; Reactive Oxygen Species/metabolism ; Superoxides
    Chemische Substanzen Fgf7 protein, mouse ; NF-E2-Related Factor 2 ; Phosphatidylinositols ; Reactive Oxygen Species ; Superoxides (11062-77-4) ; Fibroblast Growth Factor 7 (126469-10-1) ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2022-09-09
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2022.102468
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Ribosomal S6 Protein Kinase 2 Aggravates the Process of Systemic Scleroderma.

    Jiang, Mengying / Wang, Jianan / Shen, Yingjie / Zhu, Junjie / Liu, Zhili / Gong, Wenjie / Yu, Ying / Zhang, Siyi / Zhou, Xuan / He, Shengqu / Song, Yonghuan / Zhu, Zhongxin / Jin, Litai / Cong, Weitao

    The Journal of investigative dermatology

    2022  Band 142, Heft 12, Seite(n) 3175–3183.e5

    Abstract: Systemic sclerosis is a complex process of pathogenesis, and the contributions of inherited genes, infections, and chemicals remain largely unknown. In this study, we showed that p90 ribosomal S6 protein kinase 2 (RSK2) was selectively upregulated in ... ...

    Abstract Systemic sclerosis is a complex process of pathogenesis, and the contributions of inherited genes, infections, and chemicals remain largely unknown. In this study, we showed that p90 ribosomal S6 protein kinase 2 (RSK2) was selectively upregulated in fibrotic skin and fibroblasts treated with the profibrotic cytokine TGF-β. Moreover, knockout of Rsk2 specifically in skin fibroblasts or pharmacological inhibition of RSK2 attenuated skin fibrosis in a mouse model. Mechanistically, RSK2 directly interacted with glycogen synthase kinase 3β in vivo and in vitro and thereby induced phosphorylation of glycogen synthase kinase 3β at Ser9 to inhibit ubiquitination and degradation of GLI1, which promoted fibroblast differentiation and skin fibrosis. Consequently, RSK2 plays an important role in the dermal skin of systemic sclerosis. These findings provided a potential therapeutic target for systemic sclerosis.
    Mesh-Begriff(e) Animals ; Mice ; Fibroblasts/metabolism ; Fibrosis ; Phosphorylation ; Ribosomal Protein S6 Kinases, 90-kDa/metabolism ; Scleroderma, Systemic/genetics ; Scleroderma, Systemic/metabolism ; Glycogen Synthase Kinase 3 beta/metabolism
    Chemische Substanzen Ribosomal Protein S6 Kinases, 90-kDa (EC 2.7.11.1) ; ribosomal protein S6 kinase, 90kDa, polypeptide 3 (EC 2.7.11.1) ; Gsk3b protein, mouse (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2022-07-16
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 80136-7
    ISSN 1523-1747 ; 0022-202X
    ISSN (online) 1523-1747
    ISSN 0022-202X
    DOI 10.1016/j.jid.2022.06.020
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Ui VI Zs.124: Hefte anzeigen Standort:
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  5. Artikel ; Online: Fibroblast growth factor 18 alleviates stress-induced pathological cardiac hypertrophy in male mice.

    Chen, Gen / An, Ning / Shen, Jingling / Chen, Huinan / Chen, Yunjie / Sun, Jia / Hu, Zhicheng / Qiu, Junhui / Jin, Cheng / He, Shengqu / Mei, Lin / Sui, Yanru / Li, Wanqian / Chen, Peng / Guan, Xueqiang / Chu, Maoping / Wang, Yang / Jin, Litai / Kim, Kwonseop /
    Li, Xiaokun / Cong, Weitao / Wang, Xu

    Nature communications

    2023  Band 14, Heft 1, Seite(n) 1235

    Abstract: Fibroblast growth factor-18 (FGF18) has diverse organ development and damage repair roles. However, its role in cardiac homeostasis following hypertrophic stimulation remains unknown. Here we investigate the regulation and function of the FGF18 in ... ...

    Abstract Fibroblast growth factor-18 (FGF18) has diverse organ development and damage repair roles. However, its role in cardiac homeostasis following hypertrophic stimulation remains unknown. Here we investigate the regulation and function of the FGF18 in pressure overload (PO)-induced pathological cardiac hypertrophy. FGF18 heterozygous (Fgf18
    Mesh-Begriff(e) Male ; Animals ; Mice ; Chromatography, Liquid ; Tandem Mass Spectrometry ; Fibroblast Growth Factors ; Mice, Knockout ; Myocytes, Cardiac ; Cardiomegaly
    Chemische Substanzen fibroblast growth factor 18 ; Fibroblast Growth Factors (62031-54-3)
    Sprache Englisch
    Erscheinungsdatum 2023-03-04
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-36895-1
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Fibroblast growth factor 20 attenuates pathological cardiac hypertrophy by activating the SIRT1 signaling pathway.

    Chen, Yunjie / An, Ning / Zhou, Xuan / Mei, Lin / Sui, Yanru / Chen, Gen / Chen, Huinan / He, Shengqu / Jin, Cheng / Hu, Zhicheng / Li, Wanqian / Wang, Yang / Lin, Zhu / Chen, Peng / Jin, Litai / Guan, Xueqiang / Wang, Xu

    Cell death & disease

    2022  Band 13, Heft 3, Seite(n) 276

    Abstract: Cardiac hypertrophy occurs initially in response to an increased cardiac load as a compensatory mechanism to maintain cardiac output. However, sustained pathological hypertrophy can develop into heart failure and cause sudden death. Fibroblast growth ... ...

    Abstract Cardiac hypertrophy occurs initially in response to an increased cardiac load as a compensatory mechanism to maintain cardiac output. However, sustained pathological hypertrophy can develop into heart failure and cause sudden death. Fibroblast growth factor 20 (FGF20) is a member of the fibroblast growth factor family, which involved in apoptosis, aging, inflammation, and autophagy. The precise function of FGF20 in pathological cardiac hypertrophy is unclear. In this study, we demonstrated that FGF20 was significantly decreased in response to hypertrophic stimulation. In contrast, overexpression of FGF20 protected against pressure overload-induced cardiac hypertrophy. Mechanistically, we found that FGF20 upregulates SIRT1 expression, causing deacetylation of FOXO1; this effect promotes the transcription of downstream antioxidant genes, thus inhibits oxidative stress. In content, the anti-hypertrophic effect of FGF20 was largely counteracted in SIRT1-knockout mice, accompanied by an increase in oxidative stress. In summary, our findings reveal a previously unknown protective effect of FGF20 on pathological cardiac hypertrophy by reducing oxidative stress through activation of the SIRT1 signaling pathway. FGF20 is a potential novel molecular target for preventing and treating pressure overload-induced myocardial injury.
    Mesh-Begriff(e) Animals ; Cardiomegaly/metabolism ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocytes, Cardiac/metabolism ; Signal Transduction ; Sirtuin 1/genetics ; Sirtuin 1/metabolism
    Chemische Substanzen Fgf20 protein, mouse ; Fibroblast Growth Factors (62031-54-3) ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
    Sprache Englisch
    Erscheinungsdatum 2022-03-28
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-022-04724-w
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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