SGK1 regulated mitochondrial dysfunction and oxidative stress in Dox-induced cardiomyocytes by regulating Hippo pathway via NEDD4-2. (a and b) The mRNA and protein expressions of heart failure marker genes (ANP, BNP, β-MHC and Acta-1) in cardiomyocytes after treatment with Dox. (c) Cardiomyocyte viability after induction with Dox. (d) Relative mitochondrial complex activity in cardiomyocytes after Dox induction. (e) The MMP in cardiomyocytes after Dox stimulating. (f) The ATP content in cardiomyocytes with treatment of Dox. (f) Relative ROS, SOD, CAT and MDA levels in cardiomyocytes after treatment with Dox. (g) Cardiomyocyte apoptosis in cardiomyocytes with Dox treatment. (f) Relative cell apoptosis related protein expression in cardiomyocytes with stimulating by Dox. ** stands for p < 0.01 vs control; ## stands for p < 0.01 vs pcSGK1 group.

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Feb 2023

Doxorubicin (Dox) was reported to cause mitochondrial dysfunction and oxidative stress in cardiomyocytes, leading to cardiomyocyte apoptosis and ultimately heart failure. Serum and glucocorticoid inducible kinase 1 (SGK1) participates in the progression of various cardiovascular diseases. Thus, we aimed to explore the role and regulatory mechanism...