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Ferroptosis is regulated cell death characterized by iron-dependent phospholipid peroxidation, and is closely related to various diseases. System Xc -, a cystine/glutamate antiporter, and glutathione peroxidase 4 (GPX4) are the key molecules in ferroptosis. Erastin and RSL3, known as inhibitors of system Xc - and GPX4, respectively, are commonly used as ferroptosis inducers. BTB and CNC homology 1 (BACH1), a heme-binding transcription repressor, promotes pro-ferroptotic signaling, and therefore, Bach1-deficient cells are resistant to ferroptosis. Irikura et al. constructed Bach1-re-expressing immortalized mouse embryonic fibroblasts (iMEFs) from Bach1-/- mice, which induce ferroptosis simply by the depletion of 2-mercaptoethanol from the culture medium (J. Biochem. 2023; 174:239-252). Transcriptional repression by re-expressed BACH1 induces suppressed glutathione synthesis and increases labile iron. Furthermore, the ferroptosis initiated by BACH1-re-expressing iMEFs is propagated to surrounding cells. Thus, the BACH1-re-expression system is a novel and powerful tool to investigate the cellular basis of ferroptosis.
Ferroptosis is regulated cell death characterized by iron-dependent phospholipid peroxidation, and is closely related to various diseases. System Xc -, a cystine/glutamate antiporter, and glutathione peroxidase 4 (GPX4) are the key molecules in ferroptosis. Erastin and RSL3, known as inhibitors of system Xc - and GPX4, respectively, are commonly used as ferroptosis inducers. BTB and CNC homology 1 (BACH1), a heme-binding transcription repressor, promotes pro-ferroptotic signaling, and therefore, Bach1-deficient cells are resistant to ferroptosis. Irikura et al. constructed Bach1-re-expressing immortalized mouse embryonic fibroblasts (iMEFs) from Bach1-/- mice, which induce ferroptosis simply by the depletion of 2-mercaptoethanol from the culture medium (J. Biochem. 2023; 174:239-252). Transcriptional repression by re-expressed BACH1 induces suppressed glutathione synthesis and increases labile iron. Furthermore, the ferroptosis initiated by BACH1-re-expressing iMEFs is propagated to surrounding cells. Thus, the BACH1-re-expression system is a novel and powerful tool to investigate the cellular basis of ferroptosis.
Intercellular adhesion molecule 1 (ICAM-1/CD54), a transmembrane glycoprotein, has been considered as one of the most important adhesion molecules during leukocyte recruitment. It is encoded by the ICAM1 gene and plays a central role in inflammation. Its crucial role in many inflammatory diseases such as ulcerative colitis and rheumatoid arthritis are well established. Given that neuroinflammation, underscored by microglial activation, is a key element in neurodegenerative diseases such as Parkinson’s disease (PD), we investigated whether ICAM-1 has a role in this progressive neurological condition and, if so, to elucidate the underpinning mechanisms. Specifically, we were interested in the potential interaction between ICAM-1, glial cells, and ferroptosis, an iron-dependent form of cell death that has recently been implicated in PD. We conclude that there exist direct and indirect (via glial cells and T cells) influences of ICAM-1 on ferroptosis and that further elucidation of these interactions can suggest novel intervention for this devastating disease.
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