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Mechanisms of anthracycline cardiotoxicity and strategies to decrease cardiac damage Geisberg CA; Sawyer DBCurr Hypertens Rep 2010[Dec]; 12 (6): 404-10Anthracyclines are common chemotherapeutic agents used to treat many different types of cancer. Unfortunately, the use of anthracyclines is limited by their cardiotoxic effects, which may become manifest as late as 20 years from initial exposure. Studies in cells and animals suggest that the mechanism of anthracycline-induced cardiotoxicity (AIC) is multifactorial. Anthracyclines induce multiple forms of cellular injury by free radical production. In addition, anthracyclines alter nucleic acid biology by intercalation into DNA and modulate intracellular signaling, leading to cell death and the disruption of homeostatic processes such as sarcomere maintenance. In an effort to decrease AIC, many strategies have been tested, but no specific therapies are universally acknowledged to prevent or treat anthracycline-induced cardiac dysfunction. Newer imaging modalities and cardiac biomarkers may be useful in improving early detection of cardiac injury and dysfunction. As long as there is no cardiac-specific therapy for AIC, evidence suggests that high-risk patients will benefit from prophylactic treatment with neurohormonal blockade by angiotensin-converting enzyme inhibitors and beta-adrenergic receptor blockers.|Adrenergic beta-Antagonists/*therapeutic use[MESH]|Angiotensin-Converting Enzyme Inhibitors/*therapeutic use[MESH]|Animals[MESH]|Anthracyclines/*adverse effects/therapeutic use[MESH]|Antibiotics, Antineoplastic/adverse effects/therapeutic use[MESH]|Antineoplastic Protocols[MESH]|Cardiotonic Agents/*therapeutic use[MESH]|Cardiotoxins/*adverse effects/therapeutic use[MESH]|Cell Death[MESH]|Heart Diseases/*chemically induced/*metabolism/mortality/physiopathology/*therapy[MESH]|Humans[MESH]|Models, Animal[MESH]|Neoplasms/drug therapy[MESH]|Oxidative Stress[MESH]|Risk Factors[MESH]|Sarcomeres/*drug effects/metabolism/pathology[MESH]|Time[MESH] |
