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the ensuing deacetylation and nuclear retention of FoxO3a amplified the transcription of manganese superoxide dismutase and catalase, lowered reactive oxygen species in the peri-infarct border zone, and limited early-phase apoptosis ( 32 /Ser 253 expelled the factor from the nucleus, suppressing the pro-apoptotic gene Casp8, halving infarct size, and normalizing stroke volume and ejection fraction ( A third mechanistic layer involves post-transcriptional control
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