Myocardial overexpression of protein phosphatase 2A-B56α improves resistance against ischemia-reperfusion injury.

A higher phosphorylation was also observed for ERK2 in TG but did not reach statistical significance ( Fig. 4 C). 3.4 Delayed acidification during ischemia in TG cardiomyocytes Since the development and progression of I/R injury depend not only on the activation of pro-survival protein kinases during reperfusion but also on metabolic conditions during ischemia, we tested the progression of the intracellular pH value.

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