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Role of Oxidative Stress and Inflammation in Doxorubicin-Induced Cardiotoxicity: A Brief Account
Version 1
: Received: 24 May 2024 / Approved: 27 May 2024 / Online: 27 May 2024 (05:51:15 CEST)
A peer-reviewed article of this Preprint also exists.
Vitale, R.; Marzocco, S.; Popolo, A. Role of Oxidative Stress and Inflammation in Doxorubicin-Induced Cardiotoxicity: A Brief Account. Int. J. Mol. Sci. 2024, 25, 7477. Vitale, R.; Marzocco, S.; Popolo, A. Role of Oxidative Stress and Inflammation in Doxorubicin-Induced Cardiotoxicity: A Brief Account. Int. J. Mol. Sci. 2024, 25, 7477.
Abstract
Cardiotoxicity is the main side effect of several chemotherapeutic drugs. Doxorubicin (Doxo) is one of the most used anthracyclines in the treatment of many tumors, but the development of acute and chronic cardiotoxicity limits its clinical usefulness. Different studies focused only on the effects of long-term Doxo administration, but recent data show that cardiomyocyte damage is an early event induced by Doxo after a single administration that can be followed by progressive functional decline, that lead to overt heart failure. The knowledge of molecular mechanisms involved in the early stage of Doxo induced cardiotoxicity is of paramount importance to treat and/or prevent it. This review aims to illustrate several mechanisms considered to underlie Doxo-induced cardiotoxicity, such as oxidative and nitrosative stress, inflammation, and mitochondrial dysfunction. Moreover, here we report data from both in vitro and in vivo studies indicating new therapeutic possibilities to prevent Doxo-induced cardiotoxicity.
Keywords
cardiotoxicity; doxorubicin; oxidative stress; inflammation
Subject
Medicine and Pharmacology, Pharmacology and Toxicology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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