Prevention of Cardiotoxicity in the Cancer Patient
Author:
Publisher
Springer Science and Business Media LLC
Subject
Pharmacology (medical),Pharmacology
Link
http://link.springer.com/article/10.1007/s12170-017-0558-1/fulltext.html
Reference58 articles.
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3. • Zhang S, Liu X, Bawa-Khalfe T, et al. Identification of the molecular basis of doxorubicin-induced cardiotoxicity. Nat Med. 2012;18(11):1639–42. https://doi.org/10.1038/nm.2919 . Mouse model data are presented to demonstrate the paradigm that doxorubicin-induced cardiotoxicity is mediated by topoisomerase-IIβ in cardiomyocytes. Cardiomyocyte-specific topoisomerase-IIβ gene deletion protected against DNA double-strand breaks and prevented transcriptional changes that result in mitochondrial dysfunction and reactive oxygen species generation. This presents a potential upstream molecular target of therapy more appealing than previous strategies such as antioxidants and iron chelators.
4. Kersting G, Tzvetkov MV, Huse K, et al. Topoisomerase II beta expression level correlates with doxorubicin-induced apoptosis in peripheral blood cells. Naunyn Schmiedeberg’s Arch Pharmacol. 2006;374(1):21–30. https://doi.org/10.1007/s00210-006-0091-0 .
5. Herrmann J, Lerman A, Sandhu NP, Villarraga HR, Mulvagh SL, Kohli M. Evaluation and management of patients with heart disease and cancer: cardio-oncology. Mayo Clin Proc. 2014;89(9):1287–306. https://doi.org/10.1016/j.mayocp.2014.05.013 .
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