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Meanwhile, mTORC1, in nutrient-rich conditions, activates forkhead box K1/2 (FoxK1/2) which counters Foxo3-induced activation of autophagy by restricting the acetylation of histone H4 and expression of critical autophagy genes [299]
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In DKD, almost all pathogenesis is inseparable from the overactivation of ROS, which is the connection point between metabolism abnormalities and hemodynamic changes[89]
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