Redox Regulation of Nrf2 in Cisplatin-Induced Kidney Injury
Cisplatin, a potent chemotherapeutic agent, is marred by severe nephrotoxicity that is governed by mechanisms involving oxidative stress, inflammation, and apoptosis pathways. The transcription factor Nrf2, pivotal in cellular defense against oxidative stress and inflammation, is the master regulato...
Ausführliche Beschreibung
Autor*in: |
Kranti A. Mapuskar [verfasserIn] Casey F. Pulliam [verfasserIn] Diana Zepeda-Orozco [verfasserIn] Benjamin R. Griffin [verfasserIn] Muhammad Furqan [verfasserIn] Douglas R. Spitz [verfasserIn] Bryan G. Allen [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2023 |
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Übergeordnetes Werk: |
In: Antioxidants - MDPI AG, 2013, 12(2023), 1728, p 1728 |
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Übergeordnetes Werk: |
volume:12 ; year:2023 ; number:1728, p 1728 |
Links: |
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DOI / URN: |
10.3390/antiox12091728 |
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Katalog-ID: |
DOAJ093465785 |
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10.3390/antiox12091728 doi (DE-627)DOAJ093465785 (DE-599)DOAJ8263fc4547b141be827d491143e309b9 DE-627 ger DE-627 rakwb eng RM1-950 Kranti A. Mapuskar verfasserin aut Redox Regulation of Nrf2 in Cisplatin-Induced Kidney Injury 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cisplatin, a potent chemotherapeutic agent, is marred by severe nephrotoxicity that is governed by mechanisms involving oxidative stress, inflammation, and apoptosis pathways. The transcription factor Nrf2, pivotal in cellular defense against oxidative stress and inflammation, is the master regulator of the antioxidant response, upregulating antioxidants and cytoprotective genes under oxidative stress. This review discusses the mechanisms underlying chemotherapy-induced kidney injury, focusing on the role of Nrf2 in cancer therapy and its redox regulation in cisplatin-induced kidney injury. We also explore Nrf2's signaling pathways, post-translational modifications, and its involvement in autophagy, as well as examine redox-based strategies for modulating Nrf2 in cisplatin-induced kidney injury while considering the limitations and potential off-target effects of Nrf2 modulation. Understanding the redox regulation of Nrf2 in cisplatin-induced kidney injury holds significant promise for developing novel therapeutic interventions. This knowledge could provide valuable insights into potential strategies for mitigating the nephrotoxicity associated with cisplatin, ultimately enhancing the safety and efficacy of cancer treatment. oxidative stress reactive oxygen species Nrf2 chemotherapy kidney injury metabolism Therapeutics. Pharmacology Casey F. Pulliam verfasserin aut Diana Zepeda-Orozco verfasserin aut Benjamin R. Griffin verfasserin aut Muhammad Furqan verfasserin aut Douglas R. Spitz verfasserin aut Bryan G. Allen verfasserin aut In Antioxidants MDPI AG, 2013 12(2023), 1728, p 1728 (DE-627)737287578 (DE-600)2704216-9 20763921 nnns volume:12 year:2023 number:1728, p 1728 https://doi.org/10.3390/antiox12091728 kostenfrei https://doaj.org/article/8263fc4547b141be827d491143e309b9 kostenfrei https://www.mdpi.com/2076-3921/12/9/1728 kostenfrei https://doaj.org/toc/2076-3921 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_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 12 2023 1728, p 1728 |
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10.3390/antiox12091728 doi (DE-627)DOAJ093465785 (DE-599)DOAJ8263fc4547b141be827d491143e309b9 DE-627 ger DE-627 rakwb eng RM1-950 Kranti A. Mapuskar verfasserin aut Redox Regulation of Nrf2 in Cisplatin-Induced Kidney Injury 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cisplatin, a potent chemotherapeutic agent, is marred by severe nephrotoxicity that is governed by mechanisms involving oxidative stress, inflammation, and apoptosis pathways. The transcription factor Nrf2, pivotal in cellular defense against oxidative stress and inflammation, is the master regulator of the antioxidant response, upregulating antioxidants and cytoprotective genes under oxidative stress. This review discusses the mechanisms underlying chemotherapy-induced kidney injury, focusing on the role of Nrf2 in cancer therapy and its redox regulation in cisplatin-induced kidney injury. We also explore Nrf2's signaling pathways, post-translational modifications, and its involvement in autophagy, as well as examine redox-based strategies for modulating Nrf2 in cisplatin-induced kidney injury while considering the limitations and potential off-target effects of Nrf2 modulation. Understanding the redox regulation of Nrf2 in cisplatin-induced kidney injury holds significant promise for developing novel therapeutic interventions. This knowledge could provide valuable insights into potential strategies for mitigating the nephrotoxicity associated with cisplatin, ultimately enhancing the safety and efficacy of cancer treatment. oxidative stress reactive oxygen species Nrf2 chemotherapy kidney injury metabolism Therapeutics. Pharmacology Casey F. Pulliam verfasserin aut Diana Zepeda-Orozco verfasserin aut Benjamin R. Griffin verfasserin aut Muhammad Furqan verfasserin aut Douglas R. Spitz verfasserin aut Bryan G. Allen verfasserin aut In Antioxidants MDPI AG, 2013 12(2023), 1728, p 1728 (DE-627)737287578 (DE-600)2704216-9 20763921 nnns volume:12 year:2023 number:1728, p 1728 https://doi.org/10.3390/antiox12091728 kostenfrei https://doaj.org/article/8263fc4547b141be827d491143e309b9 kostenfrei https://www.mdpi.com/2076-3921/12/9/1728 kostenfrei https://doaj.org/toc/2076-3921 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_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 12 2023 1728, p 1728 |
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10.3390/antiox12091728 doi (DE-627)DOAJ093465785 (DE-599)DOAJ8263fc4547b141be827d491143e309b9 DE-627 ger DE-627 rakwb eng RM1-950 Kranti A. Mapuskar verfasserin aut Redox Regulation of Nrf2 in Cisplatin-Induced Kidney Injury 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cisplatin, a potent chemotherapeutic agent, is marred by severe nephrotoxicity that is governed by mechanisms involving oxidative stress, inflammation, and apoptosis pathways. The transcription factor Nrf2, pivotal in cellular defense against oxidative stress and inflammation, is the master regulator of the antioxidant response, upregulating antioxidants and cytoprotective genes under oxidative stress. This review discusses the mechanisms underlying chemotherapy-induced kidney injury, focusing on the role of Nrf2 in cancer therapy and its redox regulation in cisplatin-induced kidney injury. We also explore Nrf2's signaling pathways, post-translational modifications, and its involvement in autophagy, as well as examine redox-based strategies for modulating Nrf2 in cisplatin-induced kidney injury while considering the limitations and potential off-target effects of Nrf2 modulation. Understanding the redox regulation of Nrf2 in cisplatin-induced kidney injury holds significant promise for developing novel therapeutic interventions. This knowledge could provide valuable insights into potential strategies for mitigating the nephrotoxicity associated with cisplatin, ultimately enhancing the safety and efficacy of cancer treatment. oxidative stress reactive oxygen species Nrf2 chemotherapy kidney injury metabolism Therapeutics. Pharmacology Casey F. Pulliam verfasserin aut Diana Zepeda-Orozco verfasserin aut Benjamin R. Griffin verfasserin aut Muhammad Furqan verfasserin aut Douglas R. Spitz verfasserin aut Bryan G. Allen verfasserin aut In Antioxidants MDPI AG, 2013 12(2023), 1728, p 1728 (DE-627)737287578 (DE-600)2704216-9 20763921 nnns volume:12 year:2023 number:1728, p 1728 https://doi.org/10.3390/antiox12091728 kostenfrei https://doaj.org/article/8263fc4547b141be827d491143e309b9 kostenfrei https://www.mdpi.com/2076-3921/12/9/1728 kostenfrei https://doaj.org/toc/2076-3921 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_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 12 2023 1728, p 1728 |
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10.3390/antiox12091728 doi (DE-627)DOAJ093465785 (DE-599)DOAJ8263fc4547b141be827d491143e309b9 DE-627 ger DE-627 rakwb eng RM1-950 Kranti A. Mapuskar verfasserin aut Redox Regulation of Nrf2 in Cisplatin-Induced Kidney Injury 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cisplatin, a potent chemotherapeutic agent, is marred by severe nephrotoxicity that is governed by mechanisms involving oxidative stress, inflammation, and apoptosis pathways. The transcription factor Nrf2, pivotal in cellular defense against oxidative stress and inflammation, is the master regulator of the antioxidant response, upregulating antioxidants and cytoprotective genes under oxidative stress. This review discusses the mechanisms underlying chemotherapy-induced kidney injury, focusing on the role of Nrf2 in cancer therapy and its redox regulation in cisplatin-induced kidney injury. We also explore Nrf2's signaling pathways, post-translational modifications, and its involvement in autophagy, as well as examine redox-based strategies for modulating Nrf2 in cisplatin-induced kidney injury while considering the limitations and potential off-target effects of Nrf2 modulation. Understanding the redox regulation of Nrf2 in cisplatin-induced kidney injury holds significant promise for developing novel therapeutic interventions. This knowledge could provide valuable insights into potential strategies for mitigating the nephrotoxicity associated with cisplatin, ultimately enhancing the safety and efficacy of cancer treatment. oxidative stress reactive oxygen species Nrf2 chemotherapy kidney injury metabolism Therapeutics. Pharmacology Casey F. Pulliam verfasserin aut Diana Zepeda-Orozco verfasserin aut Benjamin R. Griffin verfasserin aut Muhammad Furqan verfasserin aut Douglas R. Spitz verfasserin aut Bryan G. Allen verfasserin aut In Antioxidants MDPI AG, 2013 12(2023), 1728, p 1728 (DE-627)737287578 (DE-600)2704216-9 20763921 nnns volume:12 year:2023 number:1728, p 1728 https://doi.org/10.3390/antiox12091728 kostenfrei https://doaj.org/article/8263fc4547b141be827d491143e309b9 kostenfrei https://www.mdpi.com/2076-3921/12/9/1728 kostenfrei https://doaj.org/toc/2076-3921 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_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 12 2023 1728, p 1728 |
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Redox Regulation of Nrf2 in Cisplatin-Induced Kidney Injury |
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Cisplatin, a potent chemotherapeutic agent, is marred by severe nephrotoxicity that is governed by mechanisms involving oxidative stress, inflammation, and apoptosis pathways. The transcription factor Nrf2, pivotal in cellular defense against oxidative stress and inflammation, is the master regulator of the antioxidant response, upregulating antioxidants and cytoprotective genes under oxidative stress. This review discusses the mechanisms underlying chemotherapy-induced kidney injury, focusing on the role of Nrf2 in cancer therapy and its redox regulation in cisplatin-induced kidney injury. We also explore Nrf2's signaling pathways, post-translational modifications, and its involvement in autophagy, as well as examine redox-based strategies for modulating Nrf2 in cisplatin-induced kidney injury while considering the limitations and potential off-target effects of Nrf2 modulation. Understanding the redox regulation of Nrf2 in cisplatin-induced kidney injury holds significant promise for developing novel therapeutic interventions. This knowledge could provide valuable insights into potential strategies for mitigating the nephrotoxicity associated with cisplatin, ultimately enhancing the safety and efficacy of cancer treatment. |
abstractGer |
Cisplatin, a potent chemotherapeutic agent, is marred by severe nephrotoxicity that is governed by mechanisms involving oxidative stress, inflammation, and apoptosis pathways. The transcription factor Nrf2, pivotal in cellular defense against oxidative stress and inflammation, is the master regulator of the antioxidant response, upregulating antioxidants and cytoprotective genes under oxidative stress. This review discusses the mechanisms underlying chemotherapy-induced kidney injury, focusing on the role of Nrf2 in cancer therapy and its redox regulation in cisplatin-induced kidney injury. We also explore Nrf2's signaling pathways, post-translational modifications, and its involvement in autophagy, as well as examine redox-based strategies for modulating Nrf2 in cisplatin-induced kidney injury while considering the limitations and potential off-target effects of Nrf2 modulation. Understanding the redox regulation of Nrf2 in cisplatin-induced kidney injury holds significant promise for developing novel therapeutic interventions. This knowledge could provide valuable insights into potential strategies for mitigating the nephrotoxicity associated with cisplatin, ultimately enhancing the safety and efficacy of cancer treatment. |
abstract_unstemmed |
Cisplatin, a potent chemotherapeutic agent, is marred by severe nephrotoxicity that is governed by mechanisms involving oxidative stress, inflammation, and apoptosis pathways. The transcription factor Nrf2, pivotal in cellular defense against oxidative stress and inflammation, is the master regulator of the antioxidant response, upregulating antioxidants and cytoprotective genes under oxidative stress. This review discusses the mechanisms underlying chemotherapy-induced kidney injury, focusing on the role of Nrf2 in cancer therapy and its redox regulation in cisplatin-induced kidney injury. We also explore Nrf2's signaling pathways, post-translational modifications, and its involvement in autophagy, as well as examine redox-based strategies for modulating Nrf2 in cisplatin-induced kidney injury while considering the limitations and potential off-target effects of Nrf2 modulation. Understanding the redox regulation of Nrf2 in cisplatin-induced kidney injury holds significant promise for developing novel therapeutic interventions. This knowledge could provide valuable insights into potential strategies for mitigating the nephrotoxicity associated with cisplatin, ultimately enhancing the safety and efficacy of cancer treatment. |
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7.399288 |