Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis

Background Liver ischemia/reperfusion (I/R) injury is usually caused by hepatic inflow occlusion during liver surgery, and is frequently observed during war wounds and trauma. Hepatocyte ferroptosis plays a critical role in liver I/R injury, however, it remains unclear whether this process is contro...
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Autor*in:	Jia, Kai-Wei [verfasserIn] Yao, Ren-Qi [verfasserIn] Fan, Yi-Wen [verfasserIn] Zhang, Ding-Ji [verfasserIn] Zhou, Ye [verfasserIn] Wang, Min-Jun [verfasserIn] Zhang, Li-Yuan [verfasserIn] Dong, Yue [verfasserIn] Li, Zhi-Xuan [verfasserIn] Wang, Su-Yuan [verfasserIn] Wang, Mu [verfasserIn] Li, Yun-Hui [verfasserIn] Zhang, Lu-Xin [verfasserIn] Lei, Ting [verfasserIn] Gui, Liang-Chen [verfasserIn] Lu, Shan [verfasserIn] Yang, Ying-Yun [verfasserIn] Wang, Si-Xian [verfasserIn] Yu, Yi-Zhi [verfasserIn] Yao, Yong-Ming [verfasserIn] Hou, Jin [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2024

Schlagwörter:	Ischemia/reperfusion (I/R) DExH-box helicase 58 (DHX58) Glutathione peroxidase 4 (GPX4) m A modification YT521-B homology domain containing 2 (YTHDC2)

Anmerkung:	© The Author(s) 2024

Übergeordnetes Werk:	Enthalten in: Military medical research - BioMed Central, 2014, 11(2024), 1 vom: 15. Apr.
Übergeordnetes Werk:	volume:11 ; year:2024 ; number:1 ; day:15 ; month:04

Links:	Volltext

DOI / URN:	10.1186/s40779-024-00524-9

Katalog-ID:	SPR055533108

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520			\|a Background Liver ischemia/reperfusion (I/R) injury is usually caused by hepatic inflow occlusion during liver surgery, and is frequently observed during war wounds and trauma. Hepatocyte ferroptosis plays a critical role in liver I/R injury, however, it remains unclear whether this process is controlled or regulated by members of the DEAD/DExH-box helicase (DDX/DHX) family. Methods The expression of DDX/DHX family members during liver I/R injury was screened using transcriptome analysis. Hepatocyte-specific Dhx58 knockout mice were constructed, and a partial liver I/R operation was performed. Single-cell RNA sequencing (scRNA-seq) in the liver post I/R suggested enhanced ferroptosis by Dhx58hep−/−. The mRNAs and proteins associated with DExH-box helicase 58 (DHX58) were screened using RNA immunoprecipitation-sequencing (RIP-seq) and IP-mass spectrometry (IP-MS). Results Excessive production of reactive oxygen species (ROS) decreased the expression of the IFN-stimulated gene Dhx58 in hepatocytes and promoted hepatic ferroptosis, while treatment using IFN-α increased DHX58 expression and prevented ferroptosis during liver I/R injury. Mechanistically, DHX58 with RNA-binding activity constitutively associates with the mRNA of glutathione peroxidase 4 (GPX4), a central ferroptosis suppressor, and recruits the $ m^{6} $A reader YT521-B homology domain containing 2 (YTHDC2) to promote the translation of Gpx4 mRNA in an $ m^{6} $A-dependent manner, thus enhancing GPX4 protein levels and preventing hepatic ferroptosis. Conclusions This study provides mechanistic evidence that IFN-α stimulates DHX58 to promote the translation of $ m^{6} $A-modified Gpx4 mRNA, suggesting the potential clinical application of IFN-α in the prevention of hepatic ferroptosis during liver I/R injury.
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allfields	10.1186/s40779-024-00524-9 doi (DE-627)SPR055533108 (SPR)s40779-024-00524-9-e DE-627 ger DE-627 rakwb eng 610 VZ Jia, Kai-Wei verfasserin aut Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2024 Background Liver ischemia/reperfusion (I/R) injury is usually caused by hepatic inflow occlusion during liver surgery, and is frequently observed during war wounds and trauma. Hepatocyte ferroptosis plays a critical role in liver I/R injury, however, it remains unclear whether this process is controlled or regulated by members of the DEAD/DExH-box helicase (DDX/DHX) family. Methods The expression of DDX/DHX family members during liver I/R injury was screened using transcriptome analysis. Hepatocyte-specific Dhx58 knockout mice were constructed, and a partial liver I/R operation was performed. Single-cell RNA sequencing (scRNA-seq) in the liver post I/R suggested enhanced ferroptosis by Dhx58hep−/−. The mRNAs and proteins associated with DExH-box helicase 58 (DHX58) were screened using RNA immunoprecipitation-sequencing (RIP-seq) and IP-mass spectrometry (IP-MS). Results Excessive production of reactive oxygen species (ROS) decreased the expression of the IFN-stimulated gene Dhx58 in hepatocytes and promoted hepatic ferroptosis, while treatment using IFN-α increased DHX58 expression and prevented ferroptosis during liver I/R injury. Mechanistically, DHX58 with RNA-binding activity constitutively associates with the mRNA of glutathione peroxidase 4 (GPX4), a central ferroptosis suppressor, and recruits the $ m^{6} $A reader YT521-B homology domain containing 2 (YTHDC2) to promote the translation of Gpx4 mRNA in an $ m^{6} $A-dependent manner, thus enhancing GPX4 protein levels and preventing hepatic ferroptosis. Conclusions This study provides mechanistic evidence that IFN-α stimulates DHX58 to promote the translation of $ m^{6} $A-modified Gpx4 mRNA, suggesting the potential clinical application of IFN-α in the prevention of hepatic ferroptosis during liver I/R injury. Ischemia/reperfusion (I/R) (dpeaa)DE-He213 DExH-box helicase 58 (DHX58) (dpeaa)DE-He213 Glutathione peroxidase 4 (GPX4) (dpeaa)DE-He213 m (dpeaa)DE-He213 A modification (dpeaa)DE-He213 YT521-B homology domain containing 2 (YTHDC2) (dpeaa)DE-He213 Yao, Ren-Qi verfasserin aut Fan, Yi-Wen verfasserin aut Zhang, Ding-Ji verfasserin aut Zhou, Ye verfasserin aut Wang, Min-Jun verfasserin aut Zhang, Li-Yuan verfasserin aut Dong, Yue verfasserin aut Li, Zhi-Xuan verfasserin aut Wang, Su-Yuan verfasserin aut Wang, Mu verfasserin aut Li, Yun-Hui verfasserin aut Zhang, Lu-Xin verfasserin aut Lei, Ting verfasserin aut Gui, Liang-Chen verfasserin aut Lu, Shan verfasserin aut Yang, Ying-Yun verfasserin aut Wang, Si-Xian verfasserin aut Yu, Yi-Zhi verfasserin aut Yao, Yong-Ming verfasserin aut Hou, Jin verfasserin (orcid)0000-0002-8670-517X aut Enthalten in Military medical research BioMed Central, 2014 11(2024), 1 vom: 15. Apr. (DE-627)785698213 (DE-600)2768940-2 2054-9369 nnns volume:11 year:2024 number:1 day:15 month:04 https://dx.doi.org/10.1186/s40779-024-00524-9 X:VERLAG 0 kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2446 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2024 1 15 04
spelling	10.1186/s40779-024-00524-9 doi (DE-627)SPR055533108 (SPR)s40779-024-00524-9-e DE-627 ger DE-627 rakwb eng 610 VZ Jia, Kai-Wei verfasserin aut Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2024 Background Liver ischemia/reperfusion (I/R) injury is usually caused by hepatic inflow occlusion during liver surgery, and is frequently observed during war wounds and trauma. Hepatocyte ferroptosis plays a critical role in liver I/R injury, however, it remains unclear whether this process is controlled or regulated by members of the DEAD/DExH-box helicase (DDX/DHX) family. Methods The expression of DDX/DHX family members during liver I/R injury was screened using transcriptome analysis. Hepatocyte-specific Dhx58 knockout mice were constructed, and a partial liver I/R operation was performed. Single-cell RNA sequencing (scRNA-seq) in the liver post I/R suggested enhanced ferroptosis by Dhx58hep−/−. The mRNAs and proteins associated with DExH-box helicase 58 (DHX58) were screened using RNA immunoprecipitation-sequencing (RIP-seq) and IP-mass spectrometry (IP-MS). Results Excessive production of reactive oxygen species (ROS) decreased the expression of the IFN-stimulated gene Dhx58 in hepatocytes and promoted hepatic ferroptosis, while treatment using IFN-α increased DHX58 expression and prevented ferroptosis during liver I/R injury. Mechanistically, DHX58 with RNA-binding activity constitutively associates with the mRNA of glutathione peroxidase 4 (GPX4), a central ferroptosis suppressor, and recruits the $ m^{6} $A reader YT521-B homology domain containing 2 (YTHDC2) to promote the translation of Gpx4 mRNA in an $ m^{6} $A-dependent manner, thus enhancing GPX4 protein levels and preventing hepatic ferroptosis. Conclusions This study provides mechanistic evidence that IFN-α stimulates DHX58 to promote the translation of $ m^{6} $A-modified Gpx4 mRNA, suggesting the potential clinical application of IFN-α in the prevention of hepatic ferroptosis during liver I/R injury. Ischemia/reperfusion (I/R) (dpeaa)DE-He213 DExH-box helicase 58 (DHX58) (dpeaa)DE-He213 Glutathione peroxidase 4 (GPX4) (dpeaa)DE-He213 m (dpeaa)DE-He213 A modification (dpeaa)DE-He213 YT521-B homology domain containing 2 (YTHDC2) (dpeaa)DE-He213 Yao, Ren-Qi verfasserin aut Fan, Yi-Wen verfasserin aut Zhang, Ding-Ji verfasserin aut Zhou, Ye verfasserin aut Wang, Min-Jun verfasserin aut Zhang, Li-Yuan verfasserin aut Dong, Yue verfasserin aut Li, Zhi-Xuan verfasserin aut Wang, Su-Yuan verfasserin aut Wang, Mu verfasserin aut Li, Yun-Hui verfasserin aut Zhang, Lu-Xin verfasserin aut Lei, Ting verfasserin aut Gui, Liang-Chen verfasserin aut Lu, Shan verfasserin aut Yang, Ying-Yun verfasserin aut Wang, Si-Xian verfasserin aut Yu, Yi-Zhi verfasserin aut Yao, Yong-Ming verfasserin aut Hou, Jin verfasserin (orcid)0000-0002-8670-517X aut Enthalten in Military medical research BioMed Central, 2014 11(2024), 1 vom: 15. Apr. (DE-627)785698213 (DE-600)2768940-2 2054-9369 nnns volume:11 year:2024 number:1 day:15 month:04 https://dx.doi.org/10.1186/s40779-024-00524-9 X:VERLAG 0 kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2446 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2024 1 15 04
allfields_unstemmed	10.1186/s40779-024-00524-9 doi (DE-627)SPR055533108 (SPR)s40779-024-00524-9-e DE-627 ger DE-627 rakwb eng 610 VZ Jia, Kai-Wei verfasserin aut Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2024 Background Liver ischemia/reperfusion (I/R) injury is usually caused by hepatic inflow occlusion during liver surgery, and is frequently observed during war wounds and trauma. Hepatocyte ferroptosis plays a critical role in liver I/R injury, however, it remains unclear whether this process is controlled or regulated by members of the DEAD/DExH-box helicase (DDX/DHX) family. Methods The expression of DDX/DHX family members during liver I/R injury was screened using transcriptome analysis. Hepatocyte-specific Dhx58 knockout mice were constructed, and a partial liver I/R operation was performed. Single-cell RNA sequencing (scRNA-seq) in the liver post I/R suggested enhanced ferroptosis by Dhx58hep−/−. The mRNAs and proteins associated with DExH-box helicase 58 (DHX58) were screened using RNA immunoprecipitation-sequencing (RIP-seq) and IP-mass spectrometry (IP-MS). Results Excessive production of reactive oxygen species (ROS) decreased the expression of the IFN-stimulated gene Dhx58 in hepatocytes and promoted hepatic ferroptosis, while treatment using IFN-α increased DHX58 expression and prevented ferroptosis during liver I/R injury. Mechanistically, DHX58 with RNA-binding activity constitutively associates with the mRNA of glutathione peroxidase 4 (GPX4), a central ferroptosis suppressor, and recruits the $ m^{6} $A reader YT521-B homology domain containing 2 (YTHDC2) to promote the translation of Gpx4 mRNA in an $ m^{6} $A-dependent manner, thus enhancing GPX4 protein levels and preventing hepatic ferroptosis. Conclusions This study provides mechanistic evidence that IFN-α stimulates DHX58 to promote the translation of $ m^{6} $A-modified Gpx4 mRNA, suggesting the potential clinical application of IFN-α in the prevention of hepatic ferroptosis during liver I/R injury. Ischemia/reperfusion (I/R) (dpeaa)DE-He213 DExH-box helicase 58 (DHX58) (dpeaa)DE-He213 Glutathione peroxidase 4 (GPX4) (dpeaa)DE-He213 m (dpeaa)DE-He213 A modification (dpeaa)DE-He213 YT521-B homology domain containing 2 (YTHDC2) (dpeaa)DE-He213 Yao, Ren-Qi verfasserin aut Fan, Yi-Wen verfasserin aut Zhang, Ding-Ji verfasserin aut Zhou, Ye verfasserin aut Wang, Min-Jun verfasserin aut Zhang, Li-Yuan verfasserin aut Dong, Yue verfasserin aut Li, Zhi-Xuan verfasserin aut Wang, Su-Yuan verfasserin aut Wang, Mu verfasserin aut Li, Yun-Hui verfasserin aut Zhang, Lu-Xin verfasserin aut Lei, Ting verfasserin aut Gui, Liang-Chen verfasserin aut Lu, Shan verfasserin aut Yang, Ying-Yun verfasserin aut Wang, Si-Xian verfasserin aut Yu, Yi-Zhi verfasserin aut Yao, Yong-Ming verfasserin aut Hou, Jin verfasserin (orcid)0000-0002-8670-517X aut Enthalten in Military medical research BioMed Central, 2014 11(2024), 1 vom: 15. Apr. (DE-627)785698213 (DE-600)2768940-2 2054-9369 nnns volume:11 year:2024 number:1 day:15 month:04 https://dx.doi.org/10.1186/s40779-024-00524-9 X:VERLAG 0 kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2446 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2024 1 15 04
allfieldsGer	10.1186/s40779-024-00524-9 doi (DE-627)SPR055533108 (SPR)s40779-024-00524-9-e DE-627 ger DE-627 rakwb eng 610 VZ Jia, Kai-Wei verfasserin aut Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2024 Background Liver ischemia/reperfusion (I/R) injury is usually caused by hepatic inflow occlusion during liver surgery, and is frequently observed during war wounds and trauma. Hepatocyte ferroptosis plays a critical role in liver I/R injury, however, it remains unclear whether this process is controlled or regulated by members of the DEAD/DExH-box helicase (DDX/DHX) family. Methods The expression of DDX/DHX family members during liver I/R injury was screened using transcriptome analysis. Hepatocyte-specific Dhx58 knockout mice were constructed, and a partial liver I/R operation was performed. Single-cell RNA sequencing (scRNA-seq) in the liver post I/R suggested enhanced ferroptosis by Dhx58hep−/−. The mRNAs and proteins associated with DExH-box helicase 58 (DHX58) were screened using RNA immunoprecipitation-sequencing (RIP-seq) and IP-mass spectrometry (IP-MS). Results Excessive production of reactive oxygen species (ROS) decreased the expression of the IFN-stimulated gene Dhx58 in hepatocytes and promoted hepatic ferroptosis, while treatment using IFN-α increased DHX58 expression and prevented ferroptosis during liver I/R injury. Mechanistically, DHX58 with RNA-binding activity constitutively associates with the mRNA of glutathione peroxidase 4 (GPX4), a central ferroptosis suppressor, and recruits the $ m^{6} $A reader YT521-B homology domain containing 2 (YTHDC2) to promote the translation of Gpx4 mRNA in an $ m^{6} $A-dependent manner, thus enhancing GPX4 protein levels and preventing hepatic ferroptosis. Conclusions This study provides mechanistic evidence that IFN-α stimulates DHX58 to promote the translation of $ m^{6} $A-modified Gpx4 mRNA, suggesting the potential clinical application of IFN-α in the prevention of hepatic ferroptosis during liver I/R injury. Ischemia/reperfusion (I/R) (dpeaa)DE-He213 DExH-box helicase 58 (DHX58) (dpeaa)DE-He213 Glutathione peroxidase 4 (GPX4) (dpeaa)DE-He213 m (dpeaa)DE-He213 A modification (dpeaa)DE-He213 YT521-B homology domain containing 2 (YTHDC2) (dpeaa)DE-He213 Yao, Ren-Qi verfasserin aut Fan, Yi-Wen verfasserin aut Zhang, Ding-Ji verfasserin aut Zhou, Ye verfasserin aut Wang, Min-Jun verfasserin aut Zhang, Li-Yuan verfasserin aut Dong, Yue verfasserin aut Li, Zhi-Xuan verfasserin aut Wang, Su-Yuan verfasserin aut Wang, Mu verfasserin aut Li, Yun-Hui verfasserin aut Zhang, Lu-Xin verfasserin aut Lei, Ting verfasserin aut Gui, Liang-Chen verfasserin aut Lu, Shan verfasserin aut Yang, Ying-Yun verfasserin aut Wang, Si-Xian verfasserin aut Yu, Yi-Zhi verfasserin aut Yao, Yong-Ming verfasserin aut Hou, Jin verfasserin (orcid)0000-0002-8670-517X aut Enthalten in Military medical research BioMed Central, 2014 11(2024), 1 vom: 15. Apr. (DE-627)785698213 (DE-600)2768940-2 2054-9369 nnns volume:11 year:2024 number:1 day:15 month:04 https://dx.doi.org/10.1186/s40779-024-00524-9 X:VERLAG 0 kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2446 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2024 1 15 04
allfieldsSound	10.1186/s40779-024-00524-9 doi (DE-627)SPR055533108 (SPR)s40779-024-00524-9-e DE-627 ger DE-627 rakwb eng 610 VZ Jia, Kai-Wei verfasserin aut Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2024 Background Liver ischemia/reperfusion (I/R) injury is usually caused by hepatic inflow occlusion during liver surgery, and is frequently observed during war wounds and trauma. Hepatocyte ferroptosis plays a critical role in liver I/R injury, however, it remains unclear whether this process is controlled or regulated by members of the DEAD/DExH-box helicase (DDX/DHX) family. Methods The expression of DDX/DHX family members during liver I/R injury was screened using transcriptome analysis. Hepatocyte-specific Dhx58 knockout mice were constructed, and a partial liver I/R operation was performed. Single-cell RNA sequencing (scRNA-seq) in the liver post I/R suggested enhanced ferroptosis by Dhx58hep−/−. The mRNAs and proteins associated with DExH-box helicase 58 (DHX58) were screened using RNA immunoprecipitation-sequencing (RIP-seq) and IP-mass spectrometry (IP-MS). Results Excessive production of reactive oxygen species (ROS) decreased the expression of the IFN-stimulated gene Dhx58 in hepatocytes and promoted hepatic ferroptosis, while treatment using IFN-α increased DHX58 expression and prevented ferroptosis during liver I/R injury. Mechanistically, DHX58 with RNA-binding activity constitutively associates with the mRNA of glutathione peroxidase 4 (GPX4), a central ferroptosis suppressor, and recruits the $ m^{6} $A reader YT521-B homology domain containing 2 (YTHDC2) to promote the translation of Gpx4 mRNA in an $ m^{6} $A-dependent manner, thus enhancing GPX4 protein levels and preventing hepatic ferroptosis. Conclusions This study provides mechanistic evidence that IFN-α stimulates DHX58 to promote the translation of $ m^{6} $A-modified Gpx4 mRNA, suggesting the potential clinical application of IFN-α in the prevention of hepatic ferroptosis during liver I/R injury. Ischemia/reperfusion (I/R) (dpeaa)DE-He213 DExH-box helicase 58 (DHX58) (dpeaa)DE-He213 Glutathione peroxidase 4 (GPX4) (dpeaa)DE-He213 m (dpeaa)DE-He213 A modification (dpeaa)DE-He213 YT521-B homology domain containing 2 (YTHDC2) (dpeaa)DE-He213 Yao, Ren-Qi verfasserin aut Fan, Yi-Wen verfasserin aut Zhang, Ding-Ji verfasserin aut Zhou, Ye verfasserin aut Wang, Min-Jun verfasserin aut Zhang, Li-Yuan verfasserin aut Dong, Yue verfasserin aut Li, Zhi-Xuan verfasserin aut Wang, Su-Yuan verfasserin aut Wang, Mu verfasserin aut Li, Yun-Hui verfasserin aut Zhang, Lu-Xin verfasserin aut Lei, Ting verfasserin aut Gui, Liang-Chen verfasserin aut Lu, Shan verfasserin aut Yang, Ying-Yun verfasserin aut Wang, Si-Xian verfasserin aut Yu, Yi-Zhi verfasserin aut Yao, Yong-Ming verfasserin aut Hou, Jin verfasserin (orcid)0000-0002-8670-517X aut Enthalten in Military medical research BioMed Central, 2014 11(2024), 1 vom: 15. Apr. (DE-627)785698213 (DE-600)2768940-2 2054-9369 nnns volume:11 year:2024 number:1 day:15 month:04 https://dx.doi.org/10.1186/s40779-024-00524-9 X:VERLAG 0 kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2446 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2024 1 15 04
language	English
source	Enthalten in Military medical research 11(2024), 1 vom: 15. Apr. volume:11 year:2024 number:1 day:15 month:04
sourceStr	Enthalten in Military medical research 11(2024), 1 vom: 15. Apr. volume:11 year:2024 number:1 day:15 month:04
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Ischemia/reperfusion (I/R) DExH-box helicase 58 (DHX58) Glutathione peroxidase 4 (GPX4) m A modification YT521-B homology domain containing 2 (YTHDC2)
dewey-raw	610
isfreeaccess_bool	true
container_title	Military medical research
authorswithroles_txt_mv	Jia, Kai-Wei @@aut@@ Yao, Ren-Qi @@aut@@ Fan, Yi-Wen @@aut@@ Zhang, Ding-Ji @@aut@@ Zhou, Ye @@aut@@ Wang, Min-Jun @@aut@@ Zhang, Li-Yuan @@aut@@ Dong, Yue @@aut@@ Li, Zhi-Xuan @@aut@@ Wang, Su-Yuan @@aut@@ Wang, Mu @@aut@@ Li, Yun-Hui @@aut@@ Zhang, Lu-Xin @@aut@@ Lei, Ting @@aut@@ Gui, Liang-Chen @@aut@@ Lu, Shan @@aut@@ Yang, Ying-Yun @@aut@@ Wang, Si-Xian @@aut@@ Yu, Yi-Zhi @@aut@@ Yao, Yong-Ming @@aut@@ Hou, Jin @@aut@@
publishDateDaySort_date	2024-04-15T00:00:00Z
hierarchy_top_id	785698213
dewey-sort	3610
id	SPR055533108
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000naa a22002652 4500</leader><controlfield tag="001">SPR055533108</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20240416064728.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">240416s2024 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/s40779-024-00524-9</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR055533108</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s40779-024-00524-9-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Jia, Kai-Wei</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2024</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© The Author(s) 2024</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Liver ischemia/reperfusion (I/R) injury is usually caused by hepatic inflow occlusion during liver surgery, and is frequently observed during war wounds and trauma. Hepatocyte ferroptosis plays a critical role in liver I/R injury, however, it remains unclear whether this process is controlled or regulated by members of the DEAD/DExH-box helicase (DDX/DHX) family. Methods The expression of DDX/DHX family members during liver I/R injury was screened using transcriptome analysis. Hepatocyte-specific Dhx58 knockout mice were constructed, and a partial liver I/R operation was performed. Single-cell RNA sequencing (scRNA-seq) in the liver post I/R suggested enhanced ferroptosis by Dhx58hep−/−. The mRNAs and proteins associated with DExH-box helicase 58 (DHX58) were screened using RNA immunoprecipitation-sequencing (RIP-seq) and IP-mass spectrometry (IP-MS). Results Excessive production of reactive oxygen species (ROS) decreased the expression of the IFN-stimulated gene Dhx58 in hepatocytes and promoted hepatic ferroptosis, while treatment using IFN-α increased DHX58 expression and prevented ferroptosis during liver I/R injury. Mechanistically, DHX58 with RNA-binding activity constitutively associates with the mRNA of glutathione peroxidase 4 (GPX4), a central ferroptosis suppressor, and recruits the $ m^{6} $A reader YT521-B homology domain containing 2 (YTHDC2) to promote the translation of Gpx4 mRNA in an $ m^{6} $A-dependent manner, thus enhancing GPX4 protein levels and preventing hepatic ferroptosis. 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author	Jia, Kai-Wei
spellingShingle	Jia, Kai-Wei ddc 610 misc Ischemia/reperfusion (I/R) misc DExH-box helicase 58 (DHX58) misc Glutathione peroxidase 4 (GPX4) misc m misc A modification misc YT521-B homology domain containing 2 (YTHDC2) Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis
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topic_title	610 VZ Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis Ischemia/reperfusion (I/R) (dpeaa)DE-He213 DExH-box helicase 58 (DHX58) (dpeaa)DE-He213 Glutathione peroxidase 4 (GPX4) (dpeaa)DE-He213 m (dpeaa)DE-He213 A modification (dpeaa)DE-He213 YT521-B homology domain containing 2 (YTHDC2) (dpeaa)DE-He213
topic	ddc 610 misc Ischemia/reperfusion (I/R) misc DExH-box helicase 58 (DHX58) misc Glutathione peroxidase 4 (GPX4) misc m misc A modification misc YT521-B homology domain containing 2 (YTHDC2)
topic_unstemmed	ddc 610 misc Ischemia/reperfusion (I/R) misc DExH-box helicase 58 (DHX58) misc Glutathione peroxidase 4 (GPX4) misc m misc A modification misc YT521-B homology domain containing 2 (YTHDC2)
topic_browse	ddc 610 misc Ischemia/reperfusion (I/R) misc DExH-box helicase 58 (DHX58) misc Glutathione peroxidase 4 (GPX4) misc m misc A modification misc YT521-B homology domain containing 2 (YTHDC2)
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title	Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis
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title_full	Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis
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title_sort	interferon-α stimulates dexh-box helicase 58 to prevent hepatocyte ferroptosis
title_auth	Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis
abstract	Background Liver ischemia/reperfusion (I/R) injury is usually caused by hepatic inflow occlusion during liver surgery, and is frequently observed during war wounds and trauma. Hepatocyte ferroptosis plays a critical role in liver I/R injury, however, it remains unclear whether this process is controlled or regulated by members of the DEAD/DExH-box helicase (DDX/DHX) family. Methods The expression of DDX/DHX family members during liver I/R injury was screened using transcriptome analysis. Hepatocyte-specific Dhx58 knockout mice were constructed, and a partial liver I/R operation was performed. Single-cell RNA sequencing (scRNA-seq) in the liver post I/R suggested enhanced ferroptosis by Dhx58hep−/−. The mRNAs and proteins associated with DExH-box helicase 58 (DHX58) were screened using RNA immunoprecipitation-sequencing (RIP-seq) and IP-mass spectrometry (IP-MS). Results Excessive production of reactive oxygen species (ROS) decreased the expression of the IFN-stimulated gene Dhx58 in hepatocytes and promoted hepatic ferroptosis, while treatment using IFN-α increased DHX58 expression and prevented ferroptosis during liver I/R injury. Mechanistically, DHX58 with RNA-binding activity constitutively associates with the mRNA of glutathione peroxidase 4 (GPX4), a central ferroptosis suppressor, and recruits the $ m^{6} $A reader YT521-B homology domain containing 2 (YTHDC2) to promote the translation of Gpx4 mRNA in an $ m^{6} $A-dependent manner, thus enhancing GPX4 protein levels and preventing hepatic ferroptosis. Conclusions This study provides mechanistic evidence that IFN-α stimulates DHX58 to promote the translation of $ m^{6} $A-modified Gpx4 mRNA, suggesting the potential clinical application of IFN-α in the prevention of hepatic ferroptosis during liver I/R injury. © The Author(s) 2024
abstractGer	Background Liver ischemia/reperfusion (I/R) injury is usually caused by hepatic inflow occlusion during liver surgery, and is frequently observed during war wounds and trauma. Hepatocyte ferroptosis plays a critical role in liver I/R injury, however, it remains unclear whether this process is controlled or regulated by members of the DEAD/DExH-box helicase (DDX/DHX) family. Methods The expression of DDX/DHX family members during liver I/R injury was screened using transcriptome analysis. Hepatocyte-specific Dhx58 knockout mice were constructed, and a partial liver I/R operation was performed. Single-cell RNA sequencing (scRNA-seq) in the liver post I/R suggested enhanced ferroptosis by Dhx58hep−/−. The mRNAs and proteins associated with DExH-box helicase 58 (DHX58) were screened using RNA immunoprecipitation-sequencing (RIP-seq) and IP-mass spectrometry (IP-MS). Results Excessive production of reactive oxygen species (ROS) decreased the expression of the IFN-stimulated gene Dhx58 in hepatocytes and promoted hepatic ferroptosis, while treatment using IFN-α increased DHX58 expression and prevented ferroptosis during liver I/R injury. Mechanistically, DHX58 with RNA-binding activity constitutively associates with the mRNA of glutathione peroxidase 4 (GPX4), a central ferroptosis suppressor, and recruits the $ m^{6} $A reader YT521-B homology domain containing 2 (YTHDC2) to promote the translation of Gpx4 mRNA in an $ m^{6} $A-dependent manner, thus enhancing GPX4 protein levels and preventing hepatic ferroptosis. Conclusions This study provides mechanistic evidence that IFN-α stimulates DHX58 to promote the translation of $ m^{6} $A-modified Gpx4 mRNA, suggesting the potential clinical application of IFN-α in the prevention of hepatic ferroptosis during liver I/R injury. © The Author(s) 2024
abstract_unstemmed	Background Liver ischemia/reperfusion (I/R) injury is usually caused by hepatic inflow occlusion during liver surgery, and is frequently observed during war wounds and trauma. Hepatocyte ferroptosis plays a critical role in liver I/R injury, however, it remains unclear whether this process is controlled or regulated by members of the DEAD/DExH-box helicase (DDX/DHX) family. Methods The expression of DDX/DHX family members during liver I/R injury was screened using transcriptome analysis. Hepatocyte-specific Dhx58 knockout mice were constructed, and a partial liver I/R operation was performed. Single-cell RNA sequencing (scRNA-seq) in the liver post I/R suggested enhanced ferroptosis by Dhx58hep−/−. The mRNAs and proteins associated with DExH-box helicase 58 (DHX58) were screened using RNA immunoprecipitation-sequencing (RIP-seq) and IP-mass spectrometry (IP-MS). Results Excessive production of reactive oxygen species (ROS) decreased the expression of the IFN-stimulated gene Dhx58 in hepatocytes and promoted hepatic ferroptosis, while treatment using IFN-α increased DHX58 expression and prevented ferroptosis during liver I/R injury. Mechanistically, DHX58 with RNA-binding activity constitutively associates with the mRNA of glutathione peroxidase 4 (GPX4), a central ferroptosis suppressor, and recruits the $ m^{6} $A reader YT521-B homology domain containing 2 (YTHDC2) to promote the translation of Gpx4 mRNA in an $ m^{6} $A-dependent manner, thus enhancing GPX4 protein levels and preventing hepatic ferroptosis. Conclusions This study provides mechanistic evidence that IFN-α stimulates DHX58 to promote the translation of $ m^{6} $A-modified Gpx4 mRNA, suggesting the potential clinical application of IFN-α in the prevention of hepatic ferroptosis during liver I/R injury. © The Author(s) 2024
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title_short	Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis
url	https://dx.doi.org/10.1186/s40779-024-00524-9
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author2	Yao, Ren-Qi Fan, Yi-Wen Zhang, Ding-Ji Zhou, Ye Wang, Min-Jun Zhang, Li-Yuan Dong, Yue Li, Zhi-Xuan Wang, Su-Yuan Wang, Mu Li, Yun-Hui Zhang, Lu-Xin Lei, Ting Gui, Liang-Chen Lu, Shan Yang, Ying-Yun Wang, Si-Xian Yu, Yi-Zhi Yao, Yong-Ming Hou, Jin
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up_date	2024-07-03T16:16:51.253Z
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fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000naa a22002652 4500</leader><controlfield tag="001">SPR055533108</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20240416064728.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">240416s2024 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/s40779-024-00524-9</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR055533108</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s40779-024-00524-9-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Jia, Kai-Wei</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2024</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© The Author(s) 2024</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Liver ischemia/reperfusion (I/R) injury is usually caused by hepatic inflow occlusion during liver surgery, and is frequently observed during war wounds and trauma. Hepatocyte ferroptosis plays a critical role in liver I/R injury, however, it remains unclear whether this process is controlled or regulated by members of the DEAD/DExH-box helicase (DDX/DHX) family. Methods The expression of DDX/DHX family members during liver I/R injury was screened using transcriptome analysis. Hepatocyte-specific Dhx58 knockout mice were constructed, and a partial liver I/R operation was performed. Single-cell RNA sequencing (scRNA-seq) in the liver post I/R suggested enhanced ferroptosis by Dhx58hep−/−. The mRNAs and proteins associated with DExH-box helicase 58 (DHX58) were screened using RNA immunoprecipitation-sequencing (RIP-seq) and IP-mass spectrometry (IP-MS). Results Excessive production of reactive oxygen species (ROS) decreased the expression of the IFN-stimulated gene Dhx58 in hepatocytes and promoted hepatic ferroptosis, while treatment using IFN-α increased DHX58 expression and prevented ferroptosis during liver I/R injury. Mechanistically, DHX58 with RNA-binding activity constitutively associates with the mRNA of glutathione peroxidase 4 (GPX4), a central ferroptosis suppressor, and recruits the $ m^{6} $A reader YT521-B homology domain containing 2 (YTHDC2) to promote the translation of Gpx4 mRNA in an $ m^{6} $A-dependent manner, thus enhancing GPX4 protein levels and preventing hepatic ferroptosis. Conclusions This study provides mechanistic evidence that IFN-α stimulates DHX58 to promote the translation of $ m^{6} $A-modified Gpx4 mRNA, suggesting the potential clinical application of IFN-α in the prevention of hepatic ferroptosis during liver I/R injury.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Ischemia/reperfusion (I/R)</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">DExH-box helicase 58 (DHX58)</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Glutathione peroxidase 4 (GPX4)</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">m</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">A modification</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">YT521-B homology domain containing 2 (YTHDC2)</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yao, Ren-Qi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Fan, Yi-Wen</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Ding-Ji</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhou, Ye</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Min-Jun</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Li-Yuan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dong, Yue</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Zhi-Xuan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Su-Yuan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Mu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Yun-Hui</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Lu-Xin</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lei, Ting</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Gui, Liang-Chen</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lu, Shan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yang, Ying-Yun</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Si-Xian</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yu, Yi-Zhi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yao, Yong-Ming</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hou, Jin</subfield><subfield code="e">verfasserin</subfield><subfield code="0">(orcid)0000-0002-8670-517X</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Military medical research</subfield><subfield code="d">BioMed Central, 2014</subfield><subfield code="g">11(2024), 1 vom: 15. 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Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis

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