BACH1 promotes tissue necrosis and Mycobacterium tuberculosis susceptibility
Oxidative stress triggers ferroptosis, a form of cellular necrosis characterized by iron-dependent lipid peroxidation, and has been implicated in Mycobacterium tuberculosis (Mtb) pathogenesis. We investigated whether Bach1, a transcription factor that represses multiple antioxidant genes, regulates...
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| Published in | Nature microbiology Vol. 9; no. 1; pp. 120 - 135 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
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Nature Publishing Group UK
01.01.2024
Nature Publishing Group |
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| Abstract | Oxidative stress triggers ferroptosis, a form of cellular necrosis characterized by iron-dependent lipid peroxidation, and has been implicated in
Mycobacterium tuberculosis
(Mtb) pathogenesis. We investigated whether Bach1, a transcription factor that represses multiple antioxidant genes, regulates host resistance to Mtb. We found that BACH1 expression is associated clinically with active pulmonary tuberculosis. Bach1 deletion in Mtb-infected mice increased glutathione levels and Gpx4 expression that inhibit lipid peroxidation.
Bach1
−/−
macrophages exhibited increased resistance to Mtb-induced cell death, while Mtb-infected Bach1-deficient mice displayed reduced bacterial loads, pulmonary necrosis and lipid peroxidation concurrent with increased survival. Single-cell RNA-seq analysis of lungs from Mtb-infected
Bach1
−/−
mice revealed an enrichment of genes associated with ferroptosis suppression. Bach1 depletion in Mtb-infected B6.Sst1
S
mice that display human-like necrotic lung pathology also markedly reduced necrosis and increased host resistance. These findings identify Bach1 as a key regulator of cellular and tissue necrosis and host resistance in Mtb infection.
The host transcription factor, Bach1, promotes
Mycobacterium tuberculosis
pathogenesis by inhibiting protective glutathione metabolism and antioxidant responses that prevent ferroptosis. |
|---|---|
| AbstractList | Oxidative stress triggers ferroptosis, a form of cellular necrosis characterized by iron-dependent lipid peroxidation, and has been implicated in Mycobacterium tuberculosis (Mtb) pathogenesis. We investigated whether Bach1, a transcription factor that represses multiple antioxidant genes, regulates host resistance to Mtb. We found that BACH1 expression is associated clinically with active pulmonary tuberculosis. Bach1 deletion in Mtb-infected mice increased glutathione levels and Gpx4 expression that inhibit lipid peroxidation. Bach1−/− macrophages exhibited increased resistance to Mtb-induced cell death, while Mtb-infected Bach1-deficient mice displayed reduced bacterial loads, pulmonary necrosis and lipid peroxidation concurrent with increased survival. Single-cell RNA-seq analysis of lungs from Mtb-infected Bach1−/− mice revealed an enrichment of genes associated with ferroptosis suppression. Bach1 depletion in Mtb-infected B6.Sst1S mice that display human-like necrotic lung pathology also markedly reduced necrosis and increased host resistance. These findings identify Bach1 as a key regulator of cellular and tissue necrosis and host resistance in Mtb infection.The host transcription factor, Bach1, promotes Mycobacterium tuberculosis pathogenesis by inhibiting protective glutathione metabolism and antioxidant responses that prevent ferroptosis. Oxidative stress triggers ferroptosis, a form of cellular necrosis characterized by iron-dependent lipid peroxidation, and has been implicated in Mycobacterium tuberculosis (Mtb) pathogenesis. We investigated whether Bach1, a transcription factor that represses multiple antioxidant genes, regulates host resistance to Mtb. We found that BACH1 expression is associated clinically with active pulmonary tuberculosis. Bach1 deletion in Mtb-infected mice increased glutathione levels and Gpx4 expression that inhibit lipid peroxidation. Bach1 macrophages exhibited increased resistance to Mtb-induced cell death, while Mtb-infected Bach1-deficient mice displayed reduced bacterial loads, pulmonary necrosis and lipid peroxidation concurrent with increased survival. Single-cell RNA-seq analysis of lungs from Mtb-infected Bach1 mice revealed an enrichment of genes associated with ferroptosis suppression. Bach1 depletion in Mtb-infected B6.Sst1 mice that display human-like necrotic lung pathology also markedly reduced necrosis and increased host resistance. These findings identify Bach1 as a key regulator of cellular and tissue necrosis and host resistance in Mtb infection. Oxidative stress triggers ferroptosis, a form of cellular necrosis characterized by iron-dependent lipid peroxidation, and has been implicated in Mycobacterium tuberculosis (Mtb) pathogenesis. We investigated whether Bach1, a transcription factor that represses multiple antioxidant genes, regulates host resistance to Mtb. We found that BACH1 expression is associated clinically with active pulmonary tuberculosis. Bach1 deletion in Mtb-infected mice increased glutathione levels and Gpx4 expression that inhibit lipid peroxidation. Bach1 −/− macrophages exhibited increased resistance to Mtb-induced cell death, while Mtb-infected Bach1-deficient mice displayed reduced bacterial loads, pulmonary necrosis and lipid peroxidation concurrent with increased survival. Single-cell RNA-seq analysis of lungs from Mtb-infected Bach1 −/− mice revealed an enrichment of genes associated with ferroptosis suppression. Bach1 depletion in Mtb-infected B6.Sst1 S mice that display human-like necrotic lung pathology also markedly reduced necrosis and increased host resistance. These findings identify Bach1 as a key regulator of cellular and tissue necrosis and host resistance in Mtb infection. The host transcription factor, Bach1, promotes Mycobacterium tuberculosis pathogenesis by inhibiting protective glutathione metabolism and antioxidant responses that prevent ferroptosis. Oxidative stress triggers ferroptosis, a form of cellular necrosis characterized by iron-dependent lipid peroxidation, and has been implicated in Mycobacterium tuberculosis (Mtb) pathogenesis. We investigated whether Bach1, a transcription factor that represses multiple antioxidant genes, regulates host resistance to Mtb. We found that BACH1 expression is associated clinically with active pulmonary tuberculosis. Bach1 deletion in Mtb-infected mice increased glutathione levels and Gpx4 expression that inhibit lipid peroxidation. Bach1-/- macrophages exhibited increased resistance to Mtb-induced cell death, while Mtb-infected Bach1-deficient mice displayed reduced bacterial loads, pulmonary necrosis and lipid peroxidation concurrent with increased survival. Single-cell RNA-seq analysis of lungs from Mtb-infected Bach1-/- mice revealed an enrichment of genes associated with ferroptosis suppression. Bach1 depletion in Mtb-infected B6.Sst1S mice that display human-like necrotic lung pathology also markedly reduced necrosis and increased host resistance. These findings identify Bach1 as a key regulator of cellular and tissue necrosis and host resistance in Mtb infection. Oxidative stress triggers ferroptosis, a form of cellular necrosis characterized by iron-dependent lipid peroxidation, and has been implicated in Mycobacterium tuberculosis (Mtb) pathogenesis. We investigated whether Bach1, a transcription factor that represses multiple antioxidant genes, regulates host resistance to Mtb. We found that BACH1 expression is associated clinically with active pulmonary tuberculosis. Bach1 deletion in Mtb-infected mice increased glutathione levels and Gpx4 expression that inhibit lipid peroxidation. Bach1 −/− macrophages exhibited increased resistance to Mtb-induced cell death, while Mtb-infected Bach1-deficient mice displayed reduced bacterial loads, pulmonary necrosis and lipid peroxidation concurrent with increased survival. Single-cell RNA-seq analysis of lungs from Mtb-infected Bach1 −/− mice revealed an enrichment of genes associated with ferroptosis suppression. Bach1 depletion in Mtb-infected B6.Sst1 S mice that display human-like necrotic lung pathology also markedly reduced necrosis and increased host resistance. These findings identify Bach1 as a key regulator of cellular and tissue necrosis and host resistance in Mtb infection. |
| Author | Fisher, Logan Fukutani, Eduardo Queiroz, Artur T. L. Buchanan, Jay Hilligan, Kerry L. Bomfim, Caio Cesar B. Igarashi, Kazuhiko Aberman, Kate Barreto-Duarte, Beatriz Andrade, Bruno B. Kauffman, Keith Santana, Monique Freire Cordeiro-Santos, Marcelo Santuo, Leslie Barber, Daniel L. Wilkinson, Robert J. Teixeira, Mariane Araujo Mayer-Barber, Katrin D. Gazzinelli-Guimaraes, Pedro Henrique Kramnik, Igor Scriba, Thomas Amaral, Eduardo P. Namasivayam, Sivaranjani Rocha, Clarissa Gurgel Costa, Diego L. Sher, Alan |
| Author_xml | – sequence: 1 givenname: Eduardo P. orcidid: 0000-0001-5465-8113 surname: Amaral fullname: Amaral, Eduardo P. email: eduardo.amaral@nih.gov organization: Immunobiology Section, Laboratory of Parasitic Diseases, NIAID, NIH – sequence: 2 givenname: Sivaranjani orcidid: 0000-0001-9993-1347 surname: Namasivayam fullname: Namasivayam, Sivaranjani organization: Immunobiology Section, Laboratory of Parasitic Diseases, NIAID, NIH – sequence: 3 givenname: Artur T. L. orcidid: 0000-0003-4908-9993 surname: Queiroz fullname: Queiroz, Artur T. L. organization: Laboratório de Inflamação e Biomarcadores, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ) – sequence: 4 givenname: Eduardo surname: Fukutani fullname: Fukutani, Eduardo organization: Laboratório de Inflamação e Biomarcadores, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ) – sequence: 5 givenname: Kerry L. orcidid: 0000-0003-1238-1552 surname: Hilligan fullname: Hilligan, Kerry L. organization: Immunobiology Section, Laboratory of Parasitic Diseases, NIAID, NIH – sequence: 6 givenname: Kate surname: Aberman fullname: Aberman, Kate organization: Immunobiology Section, Laboratory of Parasitic Diseases, NIAID, NIH – sequence: 7 givenname: Logan orcidid: 0000-0003-4680-1527 surname: Fisher fullname: Fisher, Logan organization: Immunobiology Section, Laboratory of Parasitic Diseases, NIAID, NIH, Immunology and Microbial Pathogenesis Program, Weill Cornell Medicine Graduate School of Medical Sciences – sequence: 8 givenname: Caio Cesar B. orcidid: 0000-0003-1998-9237 surname: Bomfim fullname: Bomfim, Caio Cesar B. organization: Immunobiology Section, Laboratory of Parasitic Diseases, NIAID, NIH – sequence: 9 givenname: Keith orcidid: 0000-0001-7208-1565 surname: Kauffman fullname: Kauffman, Keith organization: T lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institutes of Allergy and Infectious Disease, National Institutes of Health – sequence: 10 givenname: Jay surname: Buchanan fullname: Buchanan, Jay organization: T lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institutes of Allergy and Infectious Disease, National Institutes of Health – sequence: 11 givenname: Leslie surname: Santuo fullname: Santuo, Leslie organization: T lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institutes of Allergy and Infectious Disease, National Institutes of Health – sequence: 12 givenname: Pedro Henrique orcidid: 0000-0003-4932-2206 surname: Gazzinelli-Guimaraes fullname: Gazzinelli-Guimaraes, Pedro Henrique organization: Helminth Immunology Section, Laboratory of Parasitic Diseases, National Institutes of Allergy and Infectious Disease, National Institutes of Health – sequence: 13 givenname: Diego L. orcidid: 0000-0002-9440-2814 surname: Costa fullname: Costa, Diego L. organization: Immunobiology Section, Laboratory of Parasitic Diseases, NIAID, NIH, Departmento de Bioquímica e Imunologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Programa de Pós-Graduação em Imunologia Básica e Aplicada, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo – sequence: 14 givenname: Mariane Araujo surname: Teixeira fullname: Teixeira, Mariane Araujo organization: Multinational Organization Network Sponsoring Translational and Epidemiological Research (MONSTER) Initiative – sequence: 15 givenname: Beatriz surname: Barreto-Duarte fullname: Barreto-Duarte, Beatriz organization: Laboratório de Inflamação e Biomarcadores, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Multinational Organization Network Sponsoring Translational and Epidemiological Research (MONSTER) Initiative, Curso de Medicina, Universidade Salvador (UNIFACS), Laureate Universities – sequence: 16 givenname: Clarissa Gurgel orcidid: 0000-0001-8922-2985 surname: Rocha fullname: Rocha, Clarissa Gurgel organization: Department of Pathology, School of Medicine of the Federal University of Bahia, Center for Biotechnology and Cell Therapy, D’Or Institute for Research and Education (IDOR), Sao Rafael Hospital – sequence: 17 givenname: Monique Freire surname: Santana fullname: Santana, Monique Freire organization: Departmento de Ensino e Pesquisa, Fundação Centro de Controle de Oncologia do Estado do Amazonas-FCECON, Fundação Medicina Tropical Doutor Heitor Vieira Dourado, Programa de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas – sequence: 18 givenname: Marcelo orcidid: 0000-0002-7140-7145 surname: Cordeiro-Santos fullname: Cordeiro-Santos, Marcelo organization: Fundação Medicina Tropical Doutor Heitor Vieira Dourado, Programa de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas, Faculdade de Medicina, Universidade Nilton Lins – sequence: 19 givenname: Daniel L. orcidid: 0000-0001-7008-7509 surname: Barber fullname: Barber, Daniel L. organization: T lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institutes of Allergy and Infectious Disease, National Institutes of Health – sequence: 20 givenname: Robert J. orcidid: 0000-0002-2753-1800 surname: Wilkinson fullname: Wilkinson, Robert J. organization: Wellcome Centre for Infectious Disease Research in Africa, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, The Francis Crick Institute, Department of Infectious Disease, Imperial College London – sequence: 21 givenname: Igor orcidid: 0000-0001-6511-9246 surname: Kramnik fullname: Kramnik, Igor organization: Boston University School of Medicine – sequence: 22 givenname: Kazuhiko orcidid: 0000-0002-2470-2475 surname: Igarashi fullname: Igarashi, Kazuhiko organization: Department of Biochemistry, Tohoku University Graduate School of Medicine – sequence: 23 givenname: Thomas orcidid: 0000-0002-0641-1359 surname: Scriba fullname: Scriba, Thomas organization: South African Tuberculosis Vaccine Initiative, Institute of Infectious Disease and Molecular Medicine and Division of Immunology, Department of Pathology, University of Cape Town – sequence: 24 givenname: Katrin D. orcidid: 0000-0002-0311-3233 surname: Mayer-Barber fullname: Mayer-Barber, Katrin D. organization: Inflammation and Innate Immunity Unit, Laboratory of Clinical Immunology and Microbiology, NIAID, NIH – sequence: 25 givenname: Bruno B. orcidid: 0000-0001-6833-3811 surname: Andrade fullname: Andrade, Bruno B. organization: Laboratório de Inflamação e Biomarcadores, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Multinational Organization Network Sponsoring Translational and Epidemiological Research (MONSTER) Initiative, Curso de Medicina, Universidade Salvador (UNIFACS), Laureate Universities, Department of Pathology, School of Medicine of the Federal University of Bahia, Curso de Medicina, Escola Bahiana de Medicina e Saúde Pública, Faculdade de Medicina, Universidade Federal da Bahia, Curso de Medicina, Universidade Faculdade de Tecnologia e Ciências (UniFTC), Division of Infectious Diseases, Department of Medicine, Vanderbilt University School of Medicine – sequence: 26 givenname: Alan orcidid: 0000-0001-7053-2895 surname: Sher fullname: Sher, Alan email: asher@niaid.nih.gov organization: Immunobiology Section, Laboratory of Parasitic Diseases, NIAID, NIH |
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| Cites_doi | 10.1016/j.neuroscience.2020.04.014 10.1016/j.cell.2012.03.042 10.1128/mBio.03140-20 10.3171/SPI.2008.10.08488 10.1161/CIRCRESAHA.121.319540 10.3390/app11178274 10.1080/01902148.2020.1849448 10.1038/s41467-020-16143-6 10.1186/s13075-018-1568-1 10.3389/fimmu.2021.660384 10.1126/sciimmunol.aaw6693 10.1016/j.celrep.2018.06.042 10.1073/pnas.2111643118 10.1038/s41467-020-19412-6 10.1084/jem.20220504 10.1016/j.cell.2019.06.020 10.1126/sciimmunol.abf3861 10.1016/j.cell.2022.10.025 10.1016/S0140-6736(15)01316-1 10.1038/s41564-019-0578-3 10.1074/jbc.RA119.009548 10.1089/ars.2020.8124 10.1371/journal.pone.0018367 10.1016/j.cell.2017.09.021 10.3390/antiox11050861 10.1038/s41590-020-0610-z 10.1128/spectrum.02526-22 10.1016/j.micpath.2007.09.002 10.1016/j.celrep.2018.10.073 10.1186/s12885-021-08559-0 10.1016/j.chom.2018.08.001 10.1016/j.freeradbiomed.2022.06.005 10.1016/j.celrep.2020.107825 10.3389/fimmu.2018.00860 10.1172/JCI130319 10.1038/nature13489 10.1186/s12866-016-0872-7 10.1084/jem.20200887 10.1038/s41419-022-04775-z 10.1016/j.cell.2019.08.004 10.1016/j.tcb.2020.02.009 10.1096/fj.202200853RRR 10.1016/j.jbc.2021.101032 10.1016/j.cell.2017.11.048 10.1038/s41467-023-37148-x 10.1016/j.freeradbiomed.2022.11.017 10.1084/jem.20181776 10.3390/antiox9090779 |
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| References | Smulan, L. J. et al. Sirtuin 3 Downregulation in Mycobacterium tuberculosis-infected macrophages reprograms mitochondrial metabolism and promotes cell death. mBio12, e03140-20 (2021). YamadaKModulation of the secondary injury process after spinal cord injury in Bach1-deficient mice by heme oxygenase-1J. Neurosurg. Spine2008961162010.3171/SPI.2008.10.0848819035757 ZakDEA blood RNA signature for tuberculosis disease risk: a prospective cohort studyLancet2016387231223221:CAS:528:DC%2BC28XkvV2rsrw%3D10.1016/S0140-6736(15)01316-1270173105392204 Cohen, S. B. et al. Alveolar macrophages provide an early Mycobacterium tuberculosis niche and initiate dissemination. Cell Host Microbe24, 439–446 (2018). DixonSJFerroptosis: an iron-dependent form of nonapoptotic cell deathCell2012149106010721:CAS:528:DC%2BC38XnslSntrw%3D10.1016/j.cell.2012.03.042226329703367386 StockwellBRFerroptosis: a regulated cell death nexus linking metabolism, redox biology, and diseaseCell20171712732851:CAS:528:DC%2BC2sXhs1Wqs7%2FL10.1016/j.cell.2017.09.021289855605685180 Moreira-TeixeiraLMouse transcriptome reveals potential signatures of protection and pathogenesis in human tuberculosisNat. Immunol.2020214644761:CAS:528:DC%2BB3cXltVSisbg%3D10.1038/s41590-020-0610-z322058827116040 Roca, F. J., Whitworth, L. J., Redmond, S., Jones, A. A. & Ramakrishnan, L. TNF induces pathogenic programmed macrophage necrosis in tuberculosis through a mitochondrial-lysosomal-endoplasmic reticulum circuit. Cell178, 1344–1361 (2019). Mayer-BarberKDHost-directed therapy of tuberculosis based on interleukin-1 and type I interferon crosstalkNature2014511991031:CAS:528:DC%2BC2cXhtV2qtbzO10.1038/nature13489249907504809146 ShiXMycobacterium tuberculosis Rv1324 protein contributes to mycobacterial persistence and causes pathological lung injury in mice by inducing ferroptosisMicrobiol. Spectr.202311e025262210.1128/spectrum.02526-2236625672 Ahuja, M. et al. Bach1 derepression is neuroprotective in a mouse model of Parkinson’s disease. Proc. Natl Acad. Sci. USA118, e2111643118 (2021). Bhattacharya, B. et al. The integrated stress response mediates necrosis in murine Mycobacterium tuberculosis granulomas. J. Clin. Invest.131, e130319 (2021). Zhang, L., Jiang, X., Pfau, D., Ling, Y. & Nathan, C. F. Type I interferon signaling mediates Mycobacterium tuberculosis-induced macrophage death. J. Exp. Med. 218, e20200887 (2021). de Oliveira, J., Denadai, M. B. & Costa, D. L. Crosstalk between heme oxygenase-1 and iron metabolism in macrophages: implications for the modulation of inflammation and immunity. Antioxidants11, 861 (2022). Ingold, I. et al. Selenium utilization by GPX4 is required to prevent hydroperoxide-induced ferroptosis. Cell172, 409–422 (2018). JiDXType I interferon-driven susceptibility to Mycobacterium tuberculosis is mediated by IL-1RaNat. Microbiol.20194212821351:CAS:528:DC%2BC1MXhvFKgsr7O10.1038/s41564-019-0578-3316116446879852 AlamZCounter regulation of Spic by NF-kappaB and STAT signaling controls inflammation and iron metabolism in macrophagesCell Rep.2020311078251:CAS:528:DC%2BB3cXhtlegtrfF10.1016/j.celrep.2020.107825326101268944937 Global Tuberculosis Report (World Health Organization, 2022). CaiLBACH1-hemoxygenase-1 axis regulates cellular energetics and survival following sepsisFree Radic. Biol. Med.20221881341451:CAS:528:DC%2BB38XhsFyrsLnN10.1016/j.freeradbiomed.2022.06.0053569151010507736 ReddyVPFerritin H deficiency in myeloid compartments dysregulates host energy metabolism and increases susceptibility to Mycobacterium tuberculosis infectionFront. Immunol.2018986010.3389/fimmu.2018.00860297740235943674 Qiang, L. et al. A mycobacterial effector promotes ferroptosis-dependent pathogenicity and dissemination. Nat. Commun. 14, 1430 (2023). LeeJRepasyTPapavinasasundaramKSassettiCKornfeldHMycobacterium tuberculosis induces an atypical cell death mode to escape from infected macrophagesPLoS ONE20116e183671:CAS:528:DC%2BC3MXkvVeltLw%3D10.1371/journal.pone.0018367214838323069075 DangDHeme induces intestinal epithelial cell ferroptosis via mitochondrial dysfunction in transfusion-associated necrotizing enterocolitisFASEB J.202236e2264910.1096/fj.202200853RRR36383399 Rothchild, A. C. et al. Alveolar macrophages generate a noncanonical NRF2-driven transcriptional response to Mycobacterium tuberculosis in vivo. Sci. Immunol. 4, eaaw6693 (2019). Perluigi, M., Tramutola, A., Pagnotta, S., Barone, E. & Butterfield, D. A. The BACH1/Nrf2 axis in brain in Down Syndrome and transition to Alzheimer disease-like neuropathology and dementia. Antioxidants9, 779 (2020). JiGFunctional polymorphism in the NFE2L2 gene associated with tuberculosis susceptibilityFront. Immunol.20211266038410.3389/fimmu.2021.660384341089638181729 Moreira-TeixeiraLType I IFN exacerbates disease in tuberculosis-susceptible mice by inducing neutrophil-mediated lung inflammation and NETosisNat. Commun.2020111:CAS:528:DC%2BB3cXit1OqtL3E10.1038/s41467-020-19412-6331491417643080 AmaralEPThe interplay between systemic inflammation, oxidative stress, and tissue remodeling in tuberculosisAntioxid. Redox Signal.2021344714851:CAS:528:DC%2BB3MXhvFait7o%3D10.1089/ars.2020.8124325594108020551 NishizawaHFerroptosis is controlled by the coordinated transcriptional regulation of glutathione and labile iron metabolism by the transcription factor BACH1J. Biol. Chem.202029569821:CAS:528:DC%2BB3cXjsVCnurw%3D10.1074/jbc.RA119.00954831740582 StockwellBRJiangXGuWEmerging mechanisms and disease relevance of ferroptosisTrends Cell Biol.2020304784901:CAS:528:DC%2BB3cXkvVGksLk%3D10.1016/j.tcb.2020.02.009324133177230071 FlynnJLChanJImmune cell interactions in tuberculosisCell2022185468247021:CAS:528:DC%2BB38XjtVOqsb%2FE10.1016/j.cell.2022.10.02536493751 Chinta, K. C. et al. Microanatomic distribution of myeloid heme oxygenase-1 protects against free radical-mediated immunopathology in human tuberculosis. Cell Rep.25, 1938–1952 (2018). AmaralEPN-acetyl-cysteine exhibits potent anti-mycobacterial activity in addition to its known anti-oxidative functionsBMC Microbiol.20161625110.1186/s12866-016-0872-7277931045084440 AmaralEPA major role for ferroptosis in Mycobacterium tuberculosis-induced cell death and tissue necrosisJ. Exp. Med.20192165565701:CAS:528:DC%2BC1MXptVKisrk%3D10.1084/jem.20181776307870336400546 YangYInteraction between macrophages and ferroptosisCell Death Dis.2022131:CAS:528:DC%2BB38Xht1ensrvN10.1038/s41419-022-04775-z354299909013379 LiuYBTB and CNC homology 1 inhibition ameliorates fibrosis and inflammation via blocking ERK pathway in pulmonary fibrosisExp. Lung Res.202147677710.1080/01902148.2020.184944833238752 YuSZhaiJYuJYangQYangJDownregulation of BACH1 protects against cerebral ischemia/reperfusion injury through the functions of HO-1 and NQO1Neuroscience20204361541661:CAS:528:DC%2BB3cXot1Wqsrw%3D10.1016/j.neuroscience.2020.04.01432311410 Amaral, E. P. et al. GPX4 regulates cellular necrosis and host resistance in Mycobacterium tuberculosis infection. J. Exp. Med.219, e20220504 (2022). PajueloDNAD+ depletion triggers macrophage necroptosis, a cell death pathway exploited by Mycobacterium tuberculosisCell Rep.2018244294401:CAS:528:DC%2BC1cXhtlSksLvI10.1016/j.celrep.2018.06.042299961036136256 VenketaramanVGlutathione levels and immune responses in tuberculosis patientsMicrob. Pathog.2008442552611:CAS:528:DC%2BD1cXhsFyntLg%3D10.1016/j.micpath.2007.09.00217959342 HongYLinMOuDHuangZShenPA novel ferroptosis-related 12-gene signature predicts clinical prognosis and reveals immune relevancy in clear cell renal cell carcinomaBMC Cancer2021211:CAS:528:DC%2BB3MXitVKjtLbP10.1186/s12885-021-08559-0342815318290606 Kauffman, K. D. et al. PD-1 blockade exacerbates Mycobacterium tuberculosis infection in rhesus macaques. Sci. Immunol. 6, eabf3861 (2021). BeckwithKSPlasma membrane damage causes NLRP3 activation and pyroptosis during Mycobacterium tuberculosis infectionNat. Commun.2020111:CAS:528:DC%2BB3cXpt1GltLY%3D10.1038/s41467-020-16143-6323853017210277 JiaMDeletion of BACH1 attenuates atherosclerosis by reducing endothelial inflammationCirc. Res.2022130103810551:CAS:528:DC%2BB38XotlCitb0%3D10.1161/CIRCRESAHA.121.31954035196865 KishimotoDDysregulated heme oxygenase-1low M2-like macrophages augment lupus nephritis via Bach1 induced by type I interferonsArthritis Res. Ther.2018206410.1186/s13075-018-1568-1296360915894134 Cao, R. et al. Effects of glutathione diminishment on the immune responses against Mycobacterium tuberculosis infection. Appl. Sci.11, 8274 (2021). IgarashiKNishizawaHSaikiYMatsumotoMThe transcription factor BACH1 at the crossroads of cancer biology: from epithelial-mesenchymal transition to ferroptosisJ. Biol. Chem.20212971010321:CAS:528:DC%2BB3MXhvVKgu7rF10.1016/j.jbc.2021.101032343397408387770 AndersonNMSimonMCBACH1 orchestrates lung cancer metastasisCell20191782652671:CAS:528:DC%2BC1MXht1OjsrbF10.1016/j.cell.2019.06.02031257029 DavinelliSTargeting NRF2-KEAP1 axis by omega-3 fatty acids and their derivatives: emerging opportunities against aging and diseasesFree Radic. Biol. Med.20221937367501:CAS:528:DC%2BB38XivFejsrfP10.1016/j.freeradbiomed.2022.11.01736402440 BR Stockwell (1523_CR40) 2020; 30 SJ Dixon (1523_CR16) 2012; 149 V Venketaraman (1523_CR17) 2008; 44 Z Alam (1523_CR44) 2020; 31 EP Amaral (1523_CR41) 2021; 34 D Kishimoto (1523_CR43) 2018; 20 H Nishizawa (1523_CR28) 2020; 295 1523_CR22 BR Stockwell (1523_CR39) 2017; 171 JL Flynn (1523_CR4) 2022; 185 Y Liu (1523_CR26) 2021; 47 KD Mayer-Barber (1523_CR9) 2014; 511 X Shi (1523_CR15) 2023; 11 EP Amaral (1523_CR18) 2016; 16 M Jia (1523_CR25) 2022; 130 S Davinelli (1523_CR20) 2022; 193 DE Zak (1523_CR34) 2016; 387 L Cai (1523_CR27) 2022; 188 D Dang (1523_CR48) 2022; 36 1523_CR32 D Pajuelo (1523_CR6) 2018; 24 K Igarashi (1523_CR24) 2021; 297 1523_CR35 1523_CR37 VP Reddy (1523_CR23) 2018; 9 DX Ji (1523_CR36) 2019; 4 1523_CR42 1523_CR2 1523_CR1 S Yu (1523_CR31) 2020; 436 1523_CR45 1523_CR3 1523_CR46 1523_CR47 EP Amaral (1523_CR11) 2019; 216 G Ji (1523_CR21) 2021; 12 L Moreira-Teixeira (1523_CR33) 2020; 21 Y Yang (1523_CR49) 2022; 13 1523_CR19 NM Anderson (1523_CR29) 2019; 178 J Lee (1523_CR5) 2011; 6 L Moreira-Teixeira (1523_CR8) 2020; 11 K Yamada (1523_CR30) 2008; 9 KS Beckwith (1523_CR7) 2020; 11 Y Hong (1523_CR38) 2021; 21 1523_CR10 1523_CR12 1523_CR13 1523_CR14 |
| References_xml | – volume: 436 start-page: 154 year: 2020 ident: 1523_CR31 publication-title: Neuroscience doi: 10.1016/j.neuroscience.2020.04.014 contributor: fullname: S Yu – volume: 149 start-page: 1060 year: 2012 ident: 1523_CR16 publication-title: Cell doi: 10.1016/j.cell.2012.03.042 contributor: fullname: SJ Dixon – ident: 1523_CR12 doi: 10.1128/mBio.03140-20 – volume: 9 start-page: 611 year: 2008 ident: 1523_CR30 publication-title: J. Neurosurg. Spine doi: 10.3171/SPI.2008.10.08488 contributor: fullname: K Yamada – volume: 130 start-page: 1038 year: 2022 ident: 1523_CR25 publication-title: Circ. Res. doi: 10.1161/CIRCRESAHA.121.319540 contributor: fullname: M Jia – ident: 1523_CR47 doi: 10.3390/app11178274 – volume: 47 start-page: 67 year: 2021 ident: 1523_CR26 publication-title: Exp. Lung Res. doi: 10.1080/01902148.2020.1849448 contributor: fullname: Y Liu – volume: 11 year: 2020 ident: 1523_CR7 publication-title: Nat. Commun. doi: 10.1038/s41467-020-16143-6 contributor: fullname: KS Beckwith – volume: 20 start-page: 64 year: 2018 ident: 1523_CR43 publication-title: Arthritis Res. Ther. doi: 10.1186/s13075-018-1568-1 contributor: fullname: D Kishimoto – volume: 12 start-page: 660384 year: 2021 ident: 1523_CR21 publication-title: Front. Immunol. doi: 10.3389/fimmu.2021.660384 contributor: fullname: G Ji – ident: 1523_CR3 doi: 10.1126/sciimmunol.aaw6693 – volume: 24 start-page: 429 year: 2018 ident: 1523_CR6 publication-title: Cell Rep. doi: 10.1016/j.celrep.2018.06.042 contributor: fullname: D Pajuelo – ident: 1523_CR32 doi: 10.1073/pnas.2111643118 – volume: 11 year: 2020 ident: 1523_CR8 publication-title: Nat. Commun. doi: 10.1038/s41467-020-19412-6 contributor: fullname: L Moreira-Teixeira – ident: 1523_CR13 doi: 10.1084/jem.20220504 – volume: 178 start-page: 265 year: 2019 ident: 1523_CR29 publication-title: Cell doi: 10.1016/j.cell.2019.06.020 contributor: fullname: NM Anderson – ident: 1523_CR35 doi: 10.1126/sciimmunol.abf3861 – volume: 185 start-page: 4682 year: 2022 ident: 1523_CR4 publication-title: Cell doi: 10.1016/j.cell.2022.10.025 contributor: fullname: JL Flynn – volume: 387 start-page: 2312 year: 2016 ident: 1523_CR34 publication-title: Lancet doi: 10.1016/S0140-6736(15)01316-1 contributor: fullname: DE Zak – volume: 4 start-page: 2128 year: 2019 ident: 1523_CR36 publication-title: Nat. Microbiol. doi: 10.1038/s41564-019-0578-3 contributor: fullname: DX Ji – volume: 295 start-page: 69 year: 2020 ident: 1523_CR28 publication-title: J. Biol. Chem. doi: 10.1074/jbc.RA119.009548 contributor: fullname: H Nishizawa – volume: 34 start-page: 471 year: 2021 ident: 1523_CR41 publication-title: Antioxid. Redox Signal. doi: 10.1089/ars.2020.8124 contributor: fullname: EP Amaral – volume: 6 start-page: e18367 year: 2011 ident: 1523_CR5 publication-title: PLoS ONE doi: 10.1371/journal.pone.0018367 contributor: fullname: J Lee – ident: 1523_CR1 – volume: 171 start-page: 273 year: 2017 ident: 1523_CR39 publication-title: Cell doi: 10.1016/j.cell.2017.09.021 contributor: fullname: BR Stockwell – ident: 1523_CR45 doi: 10.3390/antiox11050861 – volume: 21 start-page: 464 year: 2020 ident: 1523_CR33 publication-title: Nat. Immunol. doi: 10.1038/s41590-020-0610-z contributor: fullname: L Moreira-Teixeira – volume: 11 start-page: e0252622 year: 2023 ident: 1523_CR15 publication-title: Microbiol. Spectr. doi: 10.1128/spectrum.02526-22 contributor: fullname: X Shi – volume: 44 start-page: 255 year: 2008 ident: 1523_CR17 publication-title: Microb. Pathog. doi: 10.1016/j.micpath.2007.09.002 contributor: fullname: V Venketaraman – ident: 1523_CR22 doi: 10.1016/j.celrep.2018.10.073 – volume: 21 year: 2021 ident: 1523_CR38 publication-title: BMC Cancer doi: 10.1186/s12885-021-08559-0 contributor: fullname: Y Hong – ident: 1523_CR2 doi: 10.1016/j.chom.2018.08.001 – volume: 188 start-page: 134 year: 2022 ident: 1523_CR27 publication-title: Free Radic. Biol. Med. doi: 10.1016/j.freeradbiomed.2022.06.005 contributor: fullname: L Cai – volume: 31 start-page: 107825 year: 2020 ident: 1523_CR44 publication-title: Cell Rep. doi: 10.1016/j.celrep.2020.107825 contributor: fullname: Z Alam – volume: 9 start-page: 860 year: 2018 ident: 1523_CR23 publication-title: Front. Immunol. doi: 10.3389/fimmu.2018.00860 contributor: fullname: VP Reddy – ident: 1523_CR37 doi: 10.1172/JCI130319 – volume: 511 start-page: 99 year: 2014 ident: 1523_CR9 publication-title: Nature doi: 10.1038/nature13489 contributor: fullname: KD Mayer-Barber – volume: 16 start-page: 251 year: 2016 ident: 1523_CR18 publication-title: BMC Microbiol. doi: 10.1186/s12866-016-0872-7 contributor: fullname: EP Amaral – ident: 1523_CR10 doi: 10.1084/jem.20200887 – volume: 13 year: 2022 ident: 1523_CR49 publication-title: Cell Death Dis. doi: 10.1038/s41419-022-04775-z contributor: fullname: Y Yang – ident: 1523_CR42 doi: 10.1016/j.cell.2019.08.004 – volume: 30 start-page: 478 year: 2020 ident: 1523_CR40 publication-title: Trends Cell Biol. doi: 10.1016/j.tcb.2020.02.009 contributor: fullname: BR Stockwell – volume: 36 start-page: e22649 year: 2022 ident: 1523_CR48 publication-title: FASEB J. doi: 10.1096/fj.202200853RRR contributor: fullname: D Dang – volume: 297 start-page: 101032 year: 2021 ident: 1523_CR24 publication-title: J. Biol. Chem. doi: 10.1016/j.jbc.2021.101032 contributor: fullname: K Igarashi – ident: 1523_CR46 doi: 10.1016/j.cell.2017.11.048 – ident: 1523_CR14 doi: 10.1038/s41467-023-37148-x – volume: 193 start-page: 736 year: 2022 ident: 1523_CR20 publication-title: Free Radic. Biol. Med. doi: 10.1016/j.freeradbiomed.2022.11.017 contributor: fullname: S Davinelli – volume: 216 start-page: 556 year: 2019 ident: 1523_CR11 publication-title: J. Exp. Med. doi: 10.1084/jem.20181776 contributor: fullname: EP Amaral – ident: 1523_CR19 doi: 10.3390/antiox9090779 |
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| Snippet | Oxidative stress triggers ferroptosis, a form of cellular necrosis characterized by iron-dependent lipid peroxidation, and has been implicated in
Mycobacterium... Oxidative stress triggers ferroptosis, a form of cellular necrosis characterized by iron-dependent lipid peroxidation, and has been implicated in Mycobacterium... |
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| Title | BACH1 promotes tissue necrosis and Mycobacterium tuberculosis susceptibility |
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