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Science 332 (6028): 426-427

Copyright © 2011 by the American Association for the Advancement of Science

A Cardiac Nonproliferation Treaty

Michael D. Schneider

A common basis of human mortality is the heart, arising from morphogenetic defects of the organ at birth as well as from the chronic ravages of hypertension and coronary artery disease later in life (1). A key pathological mechanism is muscle cell death, mitigated by only a scant capacity for muscle cell renewal. Rescuing cardiac muscle cell number might underlie therapeutic strategies, such as the use of antagonists of muscle cell death, stem cell grafting (now pursued in clinical trials), and activating self-repair by dormant cardiac stem cells in the heart (2). However, the genetic networks that control cardiac muscle cell number are not completely understood. On page 458 of this issue, Heallen et al. (3) provide insights into a signaling pathway that represses the cardiac cell division cycle in mice, and show that impairing this pathway can unleash cardiac cell proliferation.

British Heart Foundation Centre of Research Excellence, National Heart and Lung Institute, Imperial College London, London SW7 2AZ, UK.

E-mail: m.d.schneider{at}imperial.ac.uk


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
MST1 mutations in autosomal recessive primary immunodeficiency characterized by defective naive T-cell survival.
N. T. Nehme, J. P. Schmid, F. Debeurme, I. Andre-Schmutz, A. Lim, P. Nitschke, F. Rieux-Laucat, P. Lutz, C. Picard, N. Mahlaoui, et al. (2012)
Blood 119, 3458-3468
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