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Oxidative stress arises when there is an imbalance between oxidant generation and antioxidant capacity, leading to the accumulation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), ultimately resulting in cellular injury and dysfunction 1

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Moreover, to completely abrogate the inaccuracy and inefficiency of the screened inhibitors, end-point free energy calculations are usually computed on MD trajectory in structure-based drug design 74

Among the UPR branches, the PERK-eIF2-ATF4 signaling axis has emerged as a particularly influential regulator of cancer cell adaptation to stress