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Additionally, certain cellular events including autophagy, endoplasmic reticulum stress, inflammatory infiltration and microcirculatory dysfunction, have been found involvement with the pathogenesis of APAP-caused liver injury ( via mediating endoplasmic reticulum (ER) stress ( via mitochondrial avenue (Figure 4)

This mechanism involves a combination of oxidative stress and the formation of iron-dependent lipophilic ROS, e.g., lipid hydroperoxides

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In particular, abnormal ROS production, a functional requirement for KRAS-mediated tumorigenicity [10], is one of the major metabolic manifestations in KRAS -driven cancer