title: Twisting and ironing: doxorubicin cardiotoxicity by mitochondrial DNA damage.
abstract: Anthracyclines are active clinical agents that have multiple mechanisms of cytotoxicity. Cardiotoxicity by anthracyclines limits the therapeutic potential of these agents, but mechanisms leading to cardiotoxicity remain controversial. Transgenic mice that lack mitochondrial topoisomerase I are hypersensitive to doxorubicin cardiotoxicity, providing support for cardiotoxicity arising from damage of mitochondrial DNA.
authors.affiliation: Biomedical Sciences Department, UIC College of Medicine and Department of Biopharmaceutical Sciences, UIC College of Pharmacy, Rockford, Illinois.
authors.forename: Karin C
authors.initials: KC
authors.lastname: Nitiss
authors.affiliation: Biomedical Sciences Department, UIC College of Medicine and Department of Biopharmaceutical Sciences, UIC College of Pharmacy, Rockford, Illinois. jlnitiss@uic.edu.
authors.forename: John L
authors.initials: JL
authors.lastname: Nitiss
mesh_terms: D000818:Animals; D000903:Antibiotics, Antineoplastic / Q000633:toxicity*; D066126:Cardiotoxicity / Q000503:physiopathology*; D004249:DNA Damage; D004272:DNA, Mitochondrial / Q000187:drug effects*; D004317:Doxorubicin / Q000633:toxicity*; D006321:Heart / Q000187:drug effects*; D051379:Mice; D008822:Mice, Transgenic
chemical_list: D000903:Antibiotics, Antineoplastic; D004272:DNA, Mitochondrial; D004317:Doxorubicin