Key result
In neonatal rat cardiomyocytes, oxidative stress from H2O2 and doxorubicin induces COX-2 expression and prostacyclin formation mediated by ERK1/2 activation, which limits cell injury.
Oxidative stress-induced cardiomyocyte injury is mitigated by ERK1/2-mediated induction of COX-2 and subsequent prostacyclin formation.
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Hypothesis-generating for ERK1/2-COX-2 cardioprotection against oxidative injury; leaves open translation to in vivo models and human disease.
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Adderley et al. (1999) studied Oxidative stress-induced cardiac damage. Hydrogen peroxide (H2O2) and doxorubicin vs. Untreated cells was evaluated on COX-2 expression, ERK1/2 activation, and prostacyclin formation. In neonatal rat cardiomyocytes, oxidative stress from H2O2 and doxorubicin induces COX-2 expression and prostacyclin formation mediated by ERK1/2 activation, which limits cell injury.
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