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Sci. Signal., 24 July 2012
Vol. 5, Issue 234, p. ra52
[DOI: 10.1126/scisignal.2002918]


Editor's Summary

Keeping the Heart Safe from Radiation
The cells that make up the muscular part of the heart, or the myocardium, are generally not actively dividing. Therefore, one would not expect radiation therapy aimed at eliminating rapidly dividing cancer cells to cause heart disease. However, radiation-related heart disease is a clinically important long-term side effect of radiation therapy. The transcription factor p53 is activated in response to radiation and other DNA-damaging stresses; whether it promotes or attenuates radiation-related heart disease is unclear. Lee et al. generated mice lacking p53 in endothelial cells, the cells that line blood vessels, and whole-heart irradiation in these mice resulted in damage to the vasculature of the heart, triggering ischemia (disrupted blood flow) in the myocardium and eventual heart failure. p53 inhibitors that protect normal cells from the effects of radiation therapy have been proposed as an approach to improve the therapeutic ratio of radiation therapy, but these data suggest that combining radiation therapy with p53 inhibitors may actually increase the risk of cardiac injury.

Citation: C.-L. Lee, E. J. Moding, K. C. Cuneo, Y. Li, J. M. Sullivan, L. Mao, I. Washington, L. B. Jeffords, R. C. Rodrigues, Y. Ma, S. Das, C. D. Kontos, Y. Kim, H. A. Rockman, D. G. Kirsch, p53 Functions in Endothelial Cells to Prevent Radiation-Induced Myocardial Injury in Mice. Sci. Signal. 5, ra52 (2012).

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Science Signaling Podcast: 24 July 2012.
D. G. Kirsch, C.-L. Lee, and A. M. VanHook (2012)
Science Signaling 5, pc16
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