Mitochondria-Targeting Small Molecules Effectively Prevent Cardiotoxicity Induced by Doxorubicin

• Published in: Molecules (Basel, Switzerland) Vol. 23; no. 6; p. 1486
• Main Authors: Shi, Wei, Deng, Hongkuan, Zhang, Jianyong, Zhang, Ying, Zhang, Xiufang, Cui, Guozhen
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 19.06.2018; MDPI
• Subjects: Angina pectoris; Animals; Apoptosis; Biosynthesis; Cancer; Cardiomyocytes; Cardiomyopathy; Cardiotoxicity; Cardiotoxicity - metabolism; Cardiotoxicity - prevention & control; Chemotherapy; Doxorubicin; Doxorubicin - adverse effects; Doxorubicin - therapeutic use; Drug Delivery Systems - methods; Drug dosages; Heart attacks; Heart failure; Homeostasis; Humans; Ischemia; Kinases; Metabolism; Metabolites; Mitochondria; Mitochondria, Heart - metabolism; Mitochondrial DNA; Natural products; Neoplasms - drug therapy; Oxidative stress; Review; Rodents; small molecules; Studies; Tumors; China; cardiotoxicity; doxorubicin; mitochondria; small molecules
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules23061486

Doxorubicin (Dox) is a chemotherapeutic agent widely used for the treatment of numerous cancers. However, the clinical use of Dox is limited by its unwanted cardiotoxicity. Mitochondrial dysfunction has been associated with Dox-induced cardiotoxicity. To mitigate Dox-related cardiotoxicity, considerable successful examples of a variety of small molecules that target mitochondria to modulate Dox-induced cardiotoxicity have appeared in recent years. Here, we review the related literatures and discuss the evidence showing that mitochondria-targeting small molecules are promising cardioprotective agents against Dox-induced cardiac events.