title: New understanding in cardiotoxicity.
abstract: Interest in cardiotoxicity has dramatically increased during the past two years, leading to exciting progress in our understanding of the field. Both clinical and experimental animal studies have emphasized the role of cardiotoxicity in myocardial pathogenesis. Exploration of the cardiotoxicity of air pollution and highly active antiretroviral therapy (HAART) through experimental animal studies have led to mechanistic insights. Novel therapeutic approaches are also under development. Continued efforts to investigate the mechanisms of cardiotoxicity induced by well-known drugs and chemicals, such as Adriamycin, have also generated critical insights into cardiac response to toxicants. Recognition of the significance of cardiotoxicity in myocardial pathogenesis has resulted in the identification of many other drugs or chemicals, such as arsenic trioxide, whose cardiotoxicity is of major concern in clinical applications. Mitochondrial cardiomyopathy, along with control of myocardial cell death, has also become an extensively studied subject. Ionic transport across the inner membrane of mitochondria, especially the function of mitochondrial ATP-sensitive K+ channels and the Ca(2+)-activated K+ channels in myocardial protection against oxidative injury, has attracted a great deal of attention. Novel approaches, such as functional genomics, proteomics and metabonomics, should significantly improve our understanding of cardiotoxicity.
authors.affiliation: University of Louisville School of Medicine, Department of Medicine, 511 South Floyd Street, MDR 530, Louisville, KY 40202, USA. yjkang01@athena.louisville.edu
authors.forename: Y James
authors.initials: YJ
authors.lastname: Kang
mesh_terms: D000397:Air Pollution / Q000009:adverse effects; D000818:Animals; D023241:Antiretroviral Therapy, Highly Active / Q000009:adverse effects; D017209:Apoptosis / Q000502:physiology; D016923:Cell Death / Q000187:drug effects; D016207:Cytokines / Q000502:physiology; D064420:Drug-Related Side Effects and Adverse Reactions; D006331:Heart Diseases / Q000139:chemically induced*; D006801:Humans; D008929:Mitochondria, Heart / Q000187:drug effects; D010085:Oxidative Phosphorylation; D017382:Reactive Oxygen Species
chemical_list: D016207:Cytokines; D017382:Reactive Oxygen Species