Abstract
In recent years, the role and mechanism of long non-coding RNA (LncRNA) in cardiovascular diseases have received increasing attention. The chemotherapy agent, doxorubicin (DOX), is one of the most effective drugs for various cancers, but its efficacy is limited by its cardiotoxicity. Therefore, further exploration is required for the molecular mechanism of DOX-induced cardiotoxicity. This study intended to investigate the role of LncRNA Non-coding RNA activated by DNA damage (NORAD) in DOX-induced cardiotoxicity, for which we adopted the AC16 human cardiomyocyte cell line for the exploration. The results showed that LncRNA NORAD knockdown could increase DOX-induced cardiomyocyte apoptosis and mitochondrial ROS level. LncRNA NORAD overexpression obtained reverse results, which further validated its role in DOX-induced cardiomyocyte apoptosis and mitochondrial ROS level. Moreover, cardiotoxicity was induced in both LncRNA NORAD-knockout and wild-type mice with DOX, showing that gene knockout aggravated pathologic lesions in the myocardial tissues of mice. Taken together, LncRNA NORAD affected DOX-induced cardiotoxicity via mitochondrial apoptosis, fission (PUM-MFF), and autophagy (p53-Parkin) pathways both in vivo and in vitro.
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