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• W1872512649 abstract "Cardiac hypertrophy results from increased mechanical load on the heart and through the action of neurohumoral mediators. ERK1/2 are known to be activated in response to almost every stress- and agonist-induced hypertrophic stimulus examined to date, suggesting the straightforward hypothesis that these kinases are required for promoting the cardiac growth response. However, recent data from genetically modified mouse models suggest a more complicated picture. For example, inducible expression of dual-specificity phosphatase 6, an ERK1/2-inactivating phosphatase, eliminated ERK1/2 phosphorylation in transgenic mice, but it did not diminish the hypertrophic response to pressure overload. Similarly, Erk1-/- and Erk2+/- mice showed no reduction in stimulus-induced cardiac growth in vivo. However, blockade or deletion of cardiac ERK1/2 did predispose the heart to decompensation and failure after long-term pressure overload. Thus, ERK1/2 signaling is not to be absolutely necessary for mediating cardiac hypertrophy, although it does appear to provide critical protective effects/signals during stress-stimulation." @default.
• W1872512649 created "2016-06-24" @default.
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• W1872512649 date "2010-02-01" @default.
• W1872512649 modified "2023-10-18" @default.
• W1872512649 title "Extracellular signal-regulated kinase 1/2 (ERK1/2) signaling in cardiac hypertrophy" @default.
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• W1872512649 doi "https://doi.org/10.1111/j.1749-6632.2009.05088.x" @default.
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