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In many cases, toxicity problems appear only in the presence of additional cardiovascular disease conditions or develop months\/years following the exposure, making the diagnosis difficult. Cardiotoxic agents affecting mitochondria include several widely used anticancer drugs [anthracyclines (Doxorubicin\/Adriamycin), cisplatin, trastuzumab (Herceptin), arsenic trioxide (Trisenox), mitoxantrone (Novantrone), imatinib (Gleevec), bevacizumab (Avastin), sunitinib (Sutent), and sorafenib (Nevaxar)], antiviral compound azidothymidine (AZT, Zidovudine) and several oral antidiabetics [e.g., rosiglitazone (Avandia)]. Illicit drugs such as alcohol, cocaine, methamphetamine, ecstasy, and synthetic cannabinoids (spice, K2) may also induce mitochondria-related cardiotoxicity. Mitochondrial toxicity develops due to various mechanisms involving interference with the mitochondrial respiratory chain (e.g., uncoupling) or inhibition of the important mitochondrial enzymes (oxidative phosphorylation, Szent-Gy\u00f6rgyi-Krebs cycle, mitochondrial DNA replication, ADP\/ATP translocator). The final phase of mitochondrial dysfunction induces loss of mitochondrial membrane potential and an increase in mitochondrial oxidative\/nitrative stress, eventually culminating into cell death. This review aims to discuss the mechanisms of mitochondrion-mediated cardiotoxicity of commonly used drugs and some potential cardioprotective strategies to prevent these toxicities.<\/jats:p>","DOI":"10.1152\/ajpheart.00554.2015","type":"journal-article","created":{"date-parts":[[2015,9,18]],"date-time":"2015-09-18T23:58:24Z","timestamp":1442620704000},"page":"H1453-H1467","source":"Crossref","is-referenced-by-count":488,"title":["Drug-induced mitochondrial dysfunction and cardiotoxicity"],"prefix":"10.1152","volume":"309","author":[{"given":"Zolt\u00e1n V","family":"Varga","sequence":"first","affiliation":[{"name":"Laboratory of Cardiovascular Physiology and Tissue Injury, National Institutes of Health\/National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland;"},{"name":"Cardiometabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, 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