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Int J Biochem Cell Biol. 2009 Dec;41(12):2351-5. doi: 10.1016/j.biocel.2009.08.002. Epub 2009 Aug 8.

Cardiac hypertrophy: targeting Raf/MEK/ERK1/2-signaling.

Author information

1
Institute of Pharmacology and Toxicology, University of Würzburg, Versbacher Strasse 9, 97078 Würzburg, Germany. lorenz@toxi.uni-wuerzburg.de

Abstract

Over the past two decades, basic research has revealed a complex network of regulatory mechanisms that control the ERK1/2-signaling cascade. ERK1/2 mediate cardiac hypertrophy, a major risk factor for the development of arrhythmias, heart failure and sudden death, but also beneficial effects, e.g. protection of the heart from cell death and ischemic injury. Selective targeting of these ambiguous ERK functions could provide a powerful tool in the treatment of cardiac disease. This short review will discuss new mechanistic insights into ERK1/2-dependent development of cardiac hypertrophy and the prospect to translate this knowledge into future therapeutic strategies.

PMID:
19666137
DOI:
10.1016/j.biocel.2009.08.002
[Indexed for MEDLINE]

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