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whether contrast-induced oxidative stress acts as a direct trigger, or if other intermediates (e.g., endoplasmic reticulum stress and mitochondrial dysfunction) are involved, requires definitive validation

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On the contrary, a high level of ROS may overload the capacity of the intracellular glutathione peroxidase detoxification system and hence cause apoptosis induced by lipids peroxidation, mitochondria permeabilization, and the accumulation of fatal DNA damage [14]

These include the ligands IGF-1 and IGF-2, the IGF binding proteins IGFBPs that regulate the bioavailability of the IGFs, the level of the IGF-1R receptor and its localization, and the IRS-1 and IRS-2 adaptor proteins [97, 98]