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Despite these few differences, both the explanted heart and the mouse model had fibrosis, hypertrophy, remodeling of Ca 2+ cycling (decrease in SERCa2 levels accompanied by a compensatory increase in NCX levels), metabolic remodeling (inhibition of Akt activity coupled with upregulation of AMPK activity), and oxidative stress (increased MDA levels and low GSH/GSSG ratio)
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