Cardiac hypertrophy: targeting Raf/MEK/ERK1/2-signaling.
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.
Lorenz
Kristina
K
Institute of Pharmacology and Toxicology, University of Würzburg, Versbacher Strasse 9, 97078 Würzburg, Germany. lorenz@toxi.uni-wuerzburg.de
Schmitt
Joachim P
JP
Vidal
Marie
M
Lohse
Martin J
MJ
D000818:Animals; D030801:Animals, Genetically Modified; D017209:Apoptosis; D001145:Arrhythmias, Cardiac / Q000517:prevention & control; D006332:Cardiomegaly / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D019610:Cytoprotection; D048049:Extracellular Signal-Regulated MAP Kinases / Q000235:genetics / Q000378:metabolism*; D006333:Heart Failure / Q000517:prevention & control; D006801:Humans; D020930:MAP Kinase Kinase Kinases; D051379:Mice; D010766:Phosphorylation; D015398:Signal Transduction; D020257:Ventricular Remodeling; D048490:raf Kinases
D048490:raf Kinases; D048049:Extracellular Signal-Regulated MAP Kinases; D020930:MAP Kinase Kinase Kinases