Copyright © 2006, European Society of Cardiology
iNOS – Another cardiac target of calcineurin
Institute of Physiology, Justus Liebig University Giessen, Germany
* Corresponding author. Physiologisches Institut, Justus-Liebig Universität, Aulweg 129, 35392 Gieβen, Germany. Tel.: +49 641 9947246; fax: +49 641 9947219. Email address: gerhild.euler@physiologie.med.uni-giessen.de
Received 30 June 2006; accepted 7 July 2006
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See article by Obasanji-Blackshire et al. [3] (pages 672–683) in this issue.
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1. Calcineurin action in the heart |
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The serine–threonine kinase calcineurin was first detected in the nervous system in 1979 [1]. Twenty years later the first report about a role of calcineurin in cardiac hypertrophy appeared [2]. Since then, research on calcineurin function in the heart has strongly intensified. During these years of research, multifunctional roles of calcineurin in cardiac hypertrophy, apoptosis, contractile function, and, as now shown in this issue of Cardiovascular Research [3], preconditioning, have been revealed. These findings point to calcineurin/NFAT signaling as being a central factor in cardiac pathophysiology. However, it is still a matter of debate whether the final result of the signaling cascade is good or bad for the heart.
Several approaches have been used to characterize the role of calcineurin in cardiac hypertrophy. What became evident from these
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2. iNOS effects in the heart |
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3. Conclusions |
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  J. R. Somers, P. L. Beck, J. P. Lees-Miller, D. Roach, Y. Li, J. Guo, S. Loken, S. Zhan, L. Semeniuk, and H. J. Duff iNOS in cardiac myocytes plays a critical role in death in a murine model of hypertrophy induced by calcineurin Am J Physiol Heart Circ Physiol, September 1, 2008; 295(3): H1122 - H1131. [Abstract] [Full Text] [PDF]
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