Key result
H2O2 (50 microM) caused transient activation of ERK1/2 and p38 MAP kinases (9.6- and 9.0-fold vs control at 20 min) and sustained activation of JNK in adult rat ventricular myocytes.
H2O2 induces differential activation of MAP kinases and Na+/H+ exchanger phosphorylation, which may contribute to cardiac myocyte dysfunction during ischemia-reperfusion.
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Animal data on oxidative stress signaling in myocytes should not alter clinical practice; leaves open whether these pathways are therapeutic targets in human ischemia-reperfusion.
Wei et al. (2001) studied Cardiac myocyte dysfunction during ischemia-reperfusion. H2O2 vs. Control was evaluated on Activation of ERK1/2, p38, and JNK MAP kinases. H2O2 (50 microM) caused transient activation of ERK1/2 and p38 MAP kinases (9.6- and 9.0-fold vs control at 20 min) and sustained activation of JNK in adult rat ventricular myocytes.