{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n The BTB and CNC homolog 1 (BACH1) transcription factor is emerging as a central regulator linking cellular redox balance to diverse pathophysiological processes. In many cell types BACH1 acts as a transcriptional repressor by directly competing with the master antioxidant regulator nuclear factor erythroid 2‐related factor 2 (Nrf2) for binding to antioxidant response elements (AREs), thereby inhibiting the inducible expression of key cytoprotective genes such as heme oxygenase‐1 (HO‐1) (see, for example."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": " This repressive activity contributes to the modulation of oxidative stress responses, as BACH1 is subject to dynamic post‐translational modifications and nucleocytoplasmic shuttling in response to stress signals. For instance, oxidant or xenobiotic exposures can trigger nuclear export and tyrosine phosphorylation of BACH1, thereby alleviating its inhibition of Nrf2‐driven antioxidant gene transcription."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In addition to its role in counteracting oxidative stress, BACH1 influences cell fate decisions. It promotes ferroptosis by repressing a subset of protective genes involved in glutathione synthesis and iron metabolism"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": ", and functions as a negative modulator of p53‐dependent cellular senescence by forming repressive complexes with histone deacetylases."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": " At the tissue level, BACH1 contributes to pathological outcomes; in cancer it not only supports tumor cell survival under oxidative conditions, but also promotes invasion and metastasis by modulating metastatic gene expression such as CXCR4 and matrix metalloproteinases."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}, {"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": " In inflammatory and metabolic disorders, BACH1 dysregulation alters macrophage polarization and lipid metabolism, as evidenced by its ability to repress LDL receptor expression when acting in concert with other transcription factors."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Recent studies further indicate that BACH1 is not only regulated by intracellular redox conditions but also by circulating factors, age‐dependent signals, and even noncoding RNAs; for example, increased BACH1 expression in aged cells appears to contribute to the decline in adaptive Nrf2‐mediated responses"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": ", while aberrantly expressed circular RNAs and long noncoding RNAs that modulate BACH1 levels have been linked to cancer progression in hepatocellular carcinoma and osteosarcoma."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "15"}]}, {"type": "t", "text": " Moreover, genetic polymorphisms in the BACH1 locus are associated with susceptibility to drug‐induced liver injury"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}]}, {"type": "t", "text": ", and pharmacological or dietary interventions that promote the degradation or nuclear export of BACH1 (for example, via nitric oxide or S-1-propenylcysteine from garlic) have been proposed as strategies to enhance antioxidant defenses."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "17"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these studies highlight BACH1 as a multifaceted regulator that integrates oxidative, metabolic, and inflammatory signals to influence cell survival, differentiation, and disease progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}, {"type": "fg_f", "ref": "7"}, {"type": "fg_f", "ref": "2"}, {"type": "fg_f", "ref": "8"}, {"type": "fg_f", "ref": "19"}, {"type": "fg_f", "ref": "3"}, {"type": "fg_f", "ref": "20"}, {"type": "fg_f", "ref": "5"}, {"type": "fg_f", "ref": "21"}, {"type": "fg_f", "ref": "9"}, {"type": "fg_f", "ref": "22"}, {"type": "fg_f", "ref": "4"}, {"type": "fg_f", "ref": "13"}, {"type": "fg_f", "ref": "12"}, {"type": "fg_f", "ref": "15"}, {"type": "fg_f", "ref": "24"}, {"type": "fg_f", "ref": "11"}, {"type": "fg_fs", "start_ref": "16", "end_ref": "18"}, {"type": "fg_f", "ref": "6"}, {"type": "fg_f", "ref": "25"}]}, {"type": "t", "text": " Targeting the regulatory circuitry of BACH1 may therefore represent a promising therapeutic avenue to restore redox homeostasis and counteract disease processes ranging from cancer and inflammatory disorders to metabolic dysfunctions.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Iris Ming-Jing Xu, Robin Kit-Ho Lai, Shu-Hai Lin, et al. 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