MiR-124 attenuates doxorubicin-induced cardiac injury via inhibiting p66Shc-mediated oxidative stress |
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Affiliation: | 1. Department of Cardiology, the Affiliated Huai’an No.1 People’s Hospital of Nanjing Medical University, Huai’an 223001, China;2. Department of emergency, Nanjing Drum Tower Hospital, Nanjing 210000, China;3. Nanjing Medical Univeristy, China |
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Abstract: | Previous studies showed that miR-124 had a protective role by reducing oxidant stress and preventing cell apoptosis and autophagy. However, its role in doxorubicin-induced cardiomyopathy was less known. In our study, we confirmed increased ROS and decreased expression of miR-124 in doxorubicin-treated heart tissues and primary cardiomyocytes. The oxidative stress and cell apoptosis were alleviated by overexpressing miR-124, characterized by decreased activity of MDA and increased activity of SOD. While inhibiting miR-124 generated opposed effects. Mechanistically, our bioinformatic prediction and luciferase assay confirmed that miR-124 inhibited the expression of p66Shc, a proapoptotic signaling pathway. Our results suggested that miR-124 was hopeful to become a therapeutic target in doxorubicin-related cardiomyopathy. |
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Keywords: | MiR-124 Cardiotoxicity Oxidative stress p66Shc |
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