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Ferroptosis is a kind of iron-dependent renewal programmed death. Its main mechanism is to catalyze the unsaturated fatty acids highly expressed on the cell membrane under the effect of divalent iron, to produce lipid peroxidation, thus inducing cell death. SLC7A11 is a known iron death-related factor. It has been proved that iron death is involved in the occurrence and development of acute diseases, but the specific mechanism is unknown. The purpose of this review is to highlight the regulatory properties of SLC7A11 and gain a deeper understanding of its role in ferroptosis-related acute injury diseases. This is a narrative review. PubMed was used as the main source to randomly implement literature search strategy to index Scopus articles. No specific terms are used. Studies have shown that SLC7A11 may affect the sensitivity of cells to iron ptosis by regulating it at the transcriptional or post-transcriptional level, which is related to the pathology of many acute injury diseases, such as acute lung injury (ALI), acute kidney injury (AKI), acute liver injury, myocardial ischemia-reperfusion injury, and acute cerebral hemorrhage. In order to clarify this point, more and more researchers turn their attention to the study of the specific mechanism between SLC7A11 and ferroptosis-related acute injury diseases. In summary, this review summarized some specific mechanisms by which ferroptosis could be controlled by SLC7A11 and clarified the underlying mechanisms of a series of diseases caused by SLC7A11-associated ferroptosis. It also provided more scientific justification for the clinical application of targeting ferroptosis in preventing and treating various diseases.
Li et al. (Mon,) studied this question.