MicroRNAs in doxorubicin-induced cardiotoxicity: The DNA damage response.
| Autor: | Kawano I; Department of Physiology, Faculty of Medicine in Hradec Kralove, Charles University in Prague, Hradec Kralove, Czechia., Adamcova M; Department of Physiology, Faculty of Medicine in Hradec Kralove, Charles University in Prague, Hradec Kralove, Czechia. |
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| Jazyk: | angličtina |
| Zdroj: | Frontiers in pharmacology [Front Pharmacol] 2022 Nov 21; Vol. 13, pp. 1055911. Date of Electronic Publication: 2022 Nov 21 (Print Publication: 2022). |
| DOI: | 10.3389/fphar.2022.1055911 |
| Abstrakt: | Doxorubicin (DOX) is a chemotherapeutic drug widely used for cancer treatment, but its use is limited by cardiotoxicity. Although free radicals from redox cycling and free cellular iron have been predominant as the suggested primary pathogenic mechanism, novel evidence has pointed to topoisomerase II inhibition and resultant genotoxic stress as the more fundamental mechanism. Recently, a growing list of microRNAs (miRNAs) has been implicated in DOX-induced cardiotoxicity (DIC). This review summarizes miRNAs reported in the recent literature in the context of DIC. A particular focus is given to miRNAs that regulate cellular responses downstream to DOX-induced DNA damage, especially p53 activation, pro-survival signaling pathway inhibition (e.g., AMPK, AKT, GATA-4, and sirtuin pathways), mitochondrial dysfunction, and ferroptosis. Since these pathways are potential targets for cardioprotection against DOX, an understanding of how miRNAs participate is necessary for developing future therapies. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2022 Kawano and Adamcova.) |
| Databáze: | MEDLINE |
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