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Review
. 2011 Aug 2;124(5):642-50.
doi: 10.1161/CIRCULATIONAHA.111.021774.

Modulation of anthracycline-induced cardiotoxicity by aerobic exercise in breast cancer: current evidence and underlying mechanisms

Jessica M Scott  1 , Aarif Khakoo, John R Mackey, Mark J Haykowsky, Pamela S Douglas, Lee W Jones
Affiliations
Review

Modulation of anthracycline-induced cardiotoxicity by aerobic exercise in breast cancer: current evidence and underlying mechanisms

Jessica M Scott et al. Circulation. .
No abstract available

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Conflict of interest statement

Disclosures: The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Mechanisms underlying DOX-induced cardiotoxicity. DOX-induced generation of ROS is a central mediator of: 1) accelerated myofilament apoptosis via upregulation of p53-MAPK pathway, 2) suppression of myofilament protein synthesis via inhibition of CPCs and GATA-4, 3) alterations in cardiac energy metabolism via downregulation of PCr/ATP and AMPK, 4) ultrastructural changes to myocytes via upregulation of calpain and cytochrome c. These changes lead to left ventricular pathological hypertrophy and ultimately heart failure. DOX, doxorubicin; ROS, reactive oxygen species; mitogen activated protein kinases, MAPK; cardiac progenitor cells, CPCs; phosphocreatine, PCr; adenosine triphosphate, ATP; AMP-activated protein kinase, AMPK.
Figure 2
Figure 2
Mechanisms underlying modulation of DOX-induced cardiotoxicity through aerobic exercise. Hsp, heat shock protein; ROS, reactive oxygen species; AMP-activated protein kinase, AMPK.
See this image and copyright information in PMC

References

    1. Von Hoff DD, Layard MW, Basa P, Davis HL, Jr, Von Hoff AL, Rozencweig M, Muggia FM. Risk factors for doxorubicin-induced congestive heart failure. Ann Intern Med. 1979;91:710–717. - PubMed
    1. Swain SM, Whaley FS, Ewer MS. Congestive heart failure in patients treated with doxorubicin: a retrospective analysis of three trials. Cancer. 2003;97:2869–2879. - PubMed
    1. Jones LW, Haykowsky MJ, Swartz JJ, Douglas PS, Mackey JR. Early breast cancer therapy and cardiovascular injury. J Am Coll Cardiol. 2007;50:1435–1441. - PubMed
    1. Eisele JC, Schaefer IM, Randel Nyengaard J, Post H, Liebetanz D, Bruel A, Muhlfeld C. Effect of voluntary exercise on number and volume of cardiomyocytes and their mitochondria in the mouse left ventricle. Basic Res Cardiol. 2008;103:12–21. - PubMed
    1. Kavazis AN, McClung JM, Hood DA, Powers SK. Exercise induces a cardiac mitochondrial phenotype that resists apoptotic stimuli. Am J Physiol Heart Circ Physiol. 2008;294:H928–H935. - PubMed

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