Mitochondrial-derived ROS promote skeletal muscle autophagy and this effect is mediated, in part, through activation of AMPK and inhibition of AKT.

It has been recently reported that p53 activation can lead to the induction of PKR-eIF2alpha phosphorylation pathway. However, we demonstrate that PKR and eIF2alpha phosphorylation at serine 51 are not downstream of p53 in response to doxorubicin treatment suggesting that PKR is not a universal target of p53 as proposed.