Abstract
Ferroptosis is a recently discovered category of programmed cell death. It is much different from other types of cell death such as apoptosis, necrosis and autophagy. The main pathological feature of ferroptosis is the accumulation of iron-dependent lipid peroxidation. The typical changes in the morphological features of ferroptosis include cell volume shrinkage and increased mitochondrial membrane area. The mechanisms of ferroptosis may be mainly related to lipid peroxidation accumulation, imbalance in amino acid antioxidant system, and disturbance of iron metabolism. Besides, hypoxia-inducible factor (HIF), nuclear factor-E2-related factor 2 (Nrf2), and p53 pathway have been demonstrated to be involved in ferroptosis. At present, the molecular mechanisms of ferroptosis pathway are still unmapped. In this review, an outlook has been put forward about the crucial role of apurinic/apyrimidinic endodeoxyribonuclease 1 (APEX1) in the regulation of ferroptosis. APEX1 plays an important role in the regulation of intracellular redox balance and can be used as a potential inhibitor of ferroptotic cell death. Bioinformatics analysis indicated that the mRNA level of APEX1 is decreased in cases of ferroptosis triggered by erastin. Besides, it was found that there was a significant correlation between APEX1 and genes in the ferroptosis pathway. We have discussed the possibility to employ APEX1 inducers or inhibitors in the regulation of ferroptosis as a new strategy for the treatment of various human diseases.
Highlights
Cell death plays an important role in the development, aging, tissue homeostasis, immunity, and stress tolerance of all multicellular organisms
apyrimidinic endodeoxyribonuclease 1 (APEX1) correlated with genes in the ferroptosis pathway
We highlighted the potential roles of APEX1 in the regulation of ferroptosis
Summary
Cell death plays an important role in the development, aging, tissue homeostasis, immunity, and stress tolerance of all multicellular organisms. Trx-1 has been proven to be an inhibitor of ferroptosis [44, 45] These results suggested that APEX1 can inhibit the accumulation of lipid peroxidation by regulating the expression of antioxidant factors through the interaction with Trx-1. The relationship between APEX1 and Nrf may be involved in the redox function of APEX1, which might be directly regulating the ARE-mediated neuronal survival [60] (Figure 1) To put it in other words, important oxidative stress genes, including Txnrd, Hmox, and Gpx, which are involved in ferroptosis, will be expressed. These results implied that the crucial functions of APEX1 interacting with Nrf activates the expression of ARE and resists ferroptosis induced by ROS. These results indicated that APEX1 may be involved in ferroptosis by regulating transcription factors through its antioxidant capacity
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