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Review
. 2014 Apr 22;3(2):e000665.
doi: 10.1161/JAHA.113.000665.

Cancer therapy-induced cardiotoxicity: basic mechanisms and potential cardioprotective therapies

Virginia Shalkey Hahn  1 , Daniel J Lenihan, Bonnie Ky
Affiliations
Review

Cancer therapy-induced cardiotoxicity: basic mechanisms and potential cardioprotective therapies

Virginia Shalkey Hahn et al. J Am Heart Assoc. .
No abstract available

Keywords: anthracycline cardiotoxicity; cardiotoxicity; cardio‐oncology; sunitinib cardiotoxicity; trastuzumab cardiotoxicity.

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Figures

Figure 1.
Figure 1.
Proposed mechanisms and potential cardioprotective therapies for cardiotoxicity due to anthracyclines and ErbB inhibitors. A, Mechanisms of anthracycline‐induced cardiotoxicity. B, Potential cardioprotective therapies target the described mechanisms of cardiotoxicity. C, Mechanisms of ErbB inhibitor‐induced cardiotoxicity by trastuzumab. ACE indicates angiotensin‐converting enzyme; ERK1/2, extracellular signal‐regulated kinase 1/2; MAPK, mitogen‐activated protein kinase; NRG‐1, neuregulin‐1; PI3K, phosphoinositide 3‐kinase; Top2β, topoisomerase IIβ.
Figure 2.
Figure 2.
Proposed mechanisms of cardiotoxicity due to VEGF signaling pathway inhibitors sunitinib and sorafenib. A, Sunitinib‐ and sorafenib‐induced cardiotoxicity are secondary to multiple potential mechanisms. B, These effects are attenuated by potential cardioprotective therapies. ACE indicates angiotensin‐converting enzyme; AMPK, AMP‐activated protein kinase; LV, left ventricle; PDGFR‐β, platelet‐derived growth factor‐β; VEGF, vascular endothelial growth factor.
See this image and copyright information in PMC

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