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• W3126183762 startingPage "107428" @default.
• W3126183762 abstract "• GRX2 is induced by H/R in cardiomyocytes. • GRX2 exerts a cardioprotective role in H/R-injured cardiomyocytes. • GRX2 regulates Nrf2 signaling by the Akt/GSK-3β axis. • GRX2 protects H/R-induced cardiac injury by Nrf2. Glutaredoxin 2 (GRX2) plays a cytoprotective role under various pathological conditions. However, whether GRX2 plays a role during myocardial ischemia-reperfusion injury has not been fully elucidated. In this work, we aimed to explore the detailed role and mechanism of GRX2 in modulating hypoxia/reoxygenation (H/R)-induced cardiac injury in vitro . H/R treatment resulted in a significant increase in GRX2 expression in cardiomyocytes. GRX2 knockdown enhanced the sensitivity of cardiomyocytes to H/R-induced apoptosis, oxidative stress, and inflammation, while GRX2 up-regulation exerted a cardioprotective role in H/R-injured cardiomyocytes. Further investigations revealed that GRX2 up-regulation enhanced the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling associated with upregulation of the phosphorylation of Akt and glycogen synthase kinase-3β (GSK-3β). Akt inhibition markedly abolished GRX2-mediated activation of Nrf2, while GSK-3β inhibition reversed GRX2-knockdown-mediated inhibition of Nrf2. In addition, Nrf2 inhibition markedly abrogated GRX2-mediated protective effects against H/R-induced apoptosis, oxidative stress and inflammation. Overall, this work indicates that GRX2 protects cardiomyocytes from H/R-induced apoptosis, oxidative stress, and inflammation by enhancing Nrf2 activation via modulation of the Akt/GSK-3β axis. Our study highlights a potential relevance of GRX2 in myocardial ischemia-reperfusion injury; it may serve as an attractive target for cardioprotection." @default.
• W3126183762 created "2021-02-15" @default.
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• W3126183762 date "2021-05-01" @default.
• W3126183762 modified "2023-09-30" @default.
• W3126183762 title "Glutaredoxin 2 protects cardiomyocytes from hypoxia/reoxygenation-induced injury by suppressing apoptosis, oxidative stress, and inflammation via enhancing Nrf2 signaling" @default.
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• W3126183762 doi "https://doi.org/10.1016/j.intimp.2021.107428" @default.
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• W3126183762 hasPublicationYear "2021" @default.
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