{"title":"BACH to the ferroptosis.","authors":"Fuminori Tokunaga","doi":"10.1093/jb/mvae064","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":""},"PeriodicalIF":2.1000,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"BACH to the ferroptosis.\",\"authors\":\"Fuminori Tokunaga\",\"doi\":\"10.1093/jb/mvae064\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":15234,\"journal\":{\"name\":\"Journal of biochemistry\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":2.1000,\"publicationDate\":\"2024-09-24\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of biochemistry\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1093/jb/mvae064\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of biochemistry","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1093/jb/mvae064","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
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.
期刊介绍：
The Journal of Biochemistry founded in 1922 publishes the results of original research in the fields of Biochemistry, Molecular Biology, Cell, and Biotechnology written in English in the form of Regular Papers or Rapid Communications. A Rapid Communication is not a preliminary note, but it is, though brief, a complete and final publication. The materials described in Rapid Communications should not be included in a later paper. The Journal also publishes short reviews (JB Review) and papers solicited by the Editorial Board.
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