Nrf2 and oxidative stress in liver ischemia/reperfusion injury
In response to stress signal, nuclear factor‐erythroid 2‐related factor 2 (Nrf2) induces the expression of target genes involved in antioxidant defense and detoxification. Nrf2 activity is strictly regulated through a variety of mechanisms, including regulation of Keap1‐Nrf2 stability, transcription...
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| Veröffentlicht in: | The FEBS journal 2022-09, Vol.289 (18), p.5463-5479 |
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| creator | G. Bardallo, Raquel Panisello‐Roselló, Arnau Sanchez‐Nuno, Sergio Alva, Norma Roselló‐Catafau, Joan Carbonell, Teresa |
| description | In response to stress signal, nuclear factor‐erythroid 2‐related factor 2 (Nrf2) induces the expression of target genes involved in antioxidant defense and detoxification. Nrf2 activity is strictly regulated through a variety of mechanisms, including regulation of Keap1‐Nrf2 stability, transcriptional regulation (NF‐ĸB, ATF3, ATF4), and post‐transcriptional regulation (miRNA), evidencing that transcriptional responses of Nrf2 are critical for the maintenance of homeostasis. Ischemia‐reperfusion (IR) injury is a major cause of graft loss and dysfunction in clinical transplantation and organ resection. During the IR process, the generation of reactive oxygen species (ROS) leads to damage from oxidative stress, oxidation of biomolecules, and mitochondrial dysfunction. Oxidative stress can trigger apoptotic and necrotic cell death. Stress factors also result in the assembly of the inflammasome protein complex and the subsequent activation and secretion of proinflammatory cytokines. After Nrf2 activation, the downstream antioxidant upregulation can act as a primary cellular defense against the cytotoxic effects of oxidative stress and help to promote hepatic recovery during IR. The complex crosstalk between Nrf2 and cellular pathways in liver IR injury and the potential therapeutic target of the Nrf2 inducers will be discussed in the present review.
Nrf2 activates different cellular mechanisms in response to ischemia‐reperfusion (IR) injury in liver. IR is a major cause of graft loss and dysfunction in clinical transplantation and organ resection. During the IR process, ROS generation leads oxidative stress, inflammation and mitochondrial dysfunction. After Nrf2 activation, the downstream antioxidant upregulation can act as a primary cellular defense and help to promote hepatic recovery during IR. |
| doi_str_mv | 10.1111/febs.16336 |
| format | Article |
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Nrf2 activates different cellular mechanisms in response to ischemia‐reperfusion (IR) injury in liver. IR is a major cause of graft loss and dysfunction in clinical transplantation and organ resection. During the IR process, ROS generation leads oxidative stress, inflammation and mitochondrial dysfunction. After Nrf2 activation, the downstream antioxidant upregulation can act as a primary cellular defense and help to promote hepatic recovery during IR.</description><identifier>ISSN: 1742-464X</identifier><identifier>EISSN: 1742-4658</identifier><identifier>DOI: 10.1111/febs.16336</identifier><identifier>PMID: 34967991</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Activating transcription factor 3 ; antioxidant ; Antioxidants ; Apoptosis ; Biomolecules ; Cell death ; Cytokines ; Cytotoxicity ; Detoxification ; Gene expression ; Gene regulation ; Hepatocytes ; Homeostasis ; Inflammasomes ; Inflammation ; Injuries ; Ischemia ; ischemia‐reperfusion injury ; Liver ; miRNA ; Mitochondria ; Nrf2 ; Oxidation ; Oxidative stress ; Reactive oxygen species ; redox ; Reperfusion ; Therapeutic targets ; Transcription ; Transplantation</subject><ispartof>The FEBS journal, 2022-09, Vol.289 (18), p.5463-5479</ispartof><rights>2021 The Authors. The published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies</rights><rights>2021 The Authors. The FEBS Journal published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.</rights><rights>2021. This article is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3936-aa888b8c4b882cb77ef0ecfefea282abce2d58ca81ec835f4e2e92951804b84a3</citedby><cites>FETCH-LOGICAL-c3936-aa888b8c4b882cb77ef0ecfefea282abce2d58ca81ec835f4e2e92951804b84a3</cites><orcidid>0000-0002-7131-3667 ; 0000-0003-0645-6140</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Ffebs.16336$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Ffebs.16336$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34967991$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>G. Bardallo, Raquel</creatorcontrib><creatorcontrib>Panisello‐Roselló, Arnau</creatorcontrib><creatorcontrib>Sanchez‐Nuno, Sergio</creatorcontrib><creatorcontrib>Alva, Norma</creatorcontrib><creatorcontrib>Roselló‐Catafau, Joan</creatorcontrib><creatorcontrib>Carbonell, Teresa</creatorcontrib><title>Nrf2 and oxidative stress in liver ischemia/reperfusion injury</title><title>The FEBS journal</title><addtitle>FEBS J</addtitle><description>In response to stress signal, nuclear factor‐erythroid 2‐related factor 2 (Nrf2) induces the expression of target genes involved in antioxidant defense and detoxification. Nrf2 activity is strictly regulated through a variety of mechanisms, including regulation of Keap1‐Nrf2 stability, transcriptional regulation (NF‐ĸB, ATF3, ATF4), and post‐transcriptional regulation (miRNA), evidencing that transcriptional responses of Nrf2 are critical for the maintenance of homeostasis. Ischemia‐reperfusion (IR) injury is a major cause of graft loss and dysfunction in clinical transplantation and organ resection. During the IR process, the generation of reactive oxygen species (ROS) leads to damage from oxidative stress, oxidation of biomolecules, and mitochondrial dysfunction. Oxidative stress can trigger apoptotic and necrotic cell death. Stress factors also result in the assembly of the inflammasome protein complex and the subsequent activation and secretion of proinflammatory cytokines. After Nrf2 activation, the downstream antioxidant upregulation can act as a primary cellular defense against the cytotoxic effects of oxidative stress and help to promote hepatic recovery during IR. The complex crosstalk between Nrf2 and cellular pathways in liver IR injury and the potential therapeutic target of the Nrf2 inducers will be discussed in the present review.
Nrf2 activates different cellular mechanisms in response to ischemia‐reperfusion (IR) injury in liver. IR is a major cause of graft loss and dysfunction in clinical transplantation and organ resection. During the IR process, ROS generation leads oxidative stress, inflammation and mitochondrial dysfunction. After Nrf2 activation, the downstream antioxidant upregulation can act as a primary cellular defense and help to promote hepatic recovery during IR.</description><subject>Activating transcription factor 3</subject><subject>antioxidant</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Biomolecules</subject><subject>Cell death</subject><subject>Cytokines</subject><subject>Cytotoxicity</subject><subject>Detoxification</subject><subject>Gene expression</subject><subject>Gene regulation</subject><subject>Hepatocytes</subject><subject>Homeostasis</subject><subject>Inflammasomes</subject><subject>Inflammation</subject><subject>Injuries</subject><subject>Ischemia</subject><subject>ischemia‐reperfusion injury</subject><subject>Liver</subject><subject>miRNA</subject><subject>Mitochondria</subject><subject>Nrf2</subject><subject>Oxidation</subject><subject>Oxidative stress</subject><subject>Reactive oxygen species</subject><subject>redox</subject><subject>Reperfusion</subject><subject>Therapeutic targets</subject><subject>Transcription</subject><subject>Transplantation</subject><issn>1742-464X</issn><issn>1742-4658</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><recordid>eNp9kE9Lw0AQxRdRbK1e_AAS8CJC2uyfJLsXQUurQtGDCt6WzWYWt6RJ3W3Ufnu3pvbgwbnMDPObx-MhdIqTIQ41MlD4Ic4ozfZQH-eMxCxL-f5uZq89dOT9PEloyoQ4RD3KRJYLgfvo6sEZEqm6jJovW6qV_YDIrxx4H9k6qsLqIuv1GyysGjlYgjOtt00drvPWrY_RgVGVh5NtH6CX6eR5fBfPHm_vx9ezWFNBs1gpznnBNSs4J7rIczAJaAMGFOFEFRpImXKtOAbNaWoYEBBEpJgn4YUpOkAXne7SNe8t-JVcBFdQVaqGpvWSZDhleUoZD-j5H3TetK4O7iTJcZpxRuiGuuwo7RrvHRi5dHah3FriRG5SlZtU5U-qAT7bSrbFAsod-htjAHAHfNoK1v9Iyenk5qkT_QawkoIT</recordid><startdate>202209</startdate><enddate>202209</enddate><creator>G. Bardallo, Raquel</creator><creator>Panisello‐Roselló, Arnau</creator><creator>Sanchez‐Nuno, Sergio</creator><creator>Alva, Norma</creator><creator>Roselló‐Catafau, Joan</creator><creator>Carbonell, Teresa</creator><general>Blackwell Publishing Ltd</general><scope>24P</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7131-3667</orcidid><orcidid>https://orcid.org/0000-0003-0645-6140</orcidid></search><sort><creationdate>202209</creationdate><title>Nrf2 and oxidative stress in liver ischemia/reperfusion injury</title><author>G. Bardallo, Raquel ; Panisello‐Roselló, Arnau ; Sanchez‐Nuno, Sergio ; Alva, Norma ; Roselló‐Catafau, Joan ; Carbonell, Teresa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3936-aa888b8c4b882cb77ef0ecfefea282abce2d58ca81ec835f4e2e92951804b84a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Activating transcription factor 3</topic><topic>antioxidant</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Biomolecules</topic><topic>Cell death</topic><topic>Cytokines</topic><topic>Cytotoxicity</topic><topic>Detoxification</topic><topic>Gene expression</topic><topic>Gene regulation</topic><topic>Hepatocytes</topic><topic>Homeostasis</topic><topic>Inflammasomes</topic><topic>Inflammation</topic><topic>Injuries</topic><topic>Ischemia</topic><topic>ischemia‐reperfusion injury</topic><topic>Liver</topic><topic>miRNA</topic><topic>Mitochondria</topic><topic>Nrf2</topic><topic>Oxidation</topic><topic>Oxidative stress</topic><topic>Reactive oxygen species</topic><topic>redox</topic><topic>Reperfusion</topic><topic>Therapeutic targets</topic><topic>Transcription</topic><topic>Transplantation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>G. Bardallo, Raquel</creatorcontrib><creatorcontrib>Panisello‐Roselló, Arnau</creatorcontrib><creatorcontrib>Sanchez‐Nuno, Sergio</creatorcontrib><creatorcontrib>Alva, Norma</creatorcontrib><creatorcontrib>Roselló‐Catafau, Joan</creatorcontrib><creatorcontrib>Carbonell, Teresa</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The FEBS journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>G. Bardallo, Raquel</au><au>Panisello‐Roselló, Arnau</au><au>Sanchez‐Nuno, Sergio</au><au>Alva, Norma</au><au>Roselló‐Catafau, Joan</au><au>Carbonell, Teresa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nrf2 and oxidative stress in liver ischemia/reperfusion injury</atitle><jtitle>The FEBS journal</jtitle><addtitle>FEBS J</addtitle><date>2022-09</date><risdate>2022</risdate><volume>289</volume><issue>18</issue><spage>5463</spage><epage>5479</epage><pages>5463-5479</pages><issn>1742-464X</issn><eissn>1742-4658</eissn><abstract>In response to stress signal, nuclear factor‐erythroid 2‐related factor 2 (Nrf2) induces the expression of target genes involved in antioxidant defense and detoxification. Nrf2 activity is strictly regulated through a variety of mechanisms, including regulation of Keap1‐Nrf2 stability, transcriptional regulation (NF‐ĸB, ATF3, ATF4), and post‐transcriptional regulation (miRNA), evidencing that transcriptional responses of Nrf2 are critical for the maintenance of homeostasis. Ischemia‐reperfusion (IR) injury is a major cause of graft loss and dysfunction in clinical transplantation and organ resection. During the IR process, the generation of reactive oxygen species (ROS) leads to damage from oxidative stress, oxidation of biomolecules, and mitochondrial dysfunction. Oxidative stress can trigger apoptotic and necrotic cell death. Stress factors also result in the assembly of the inflammasome protein complex and the subsequent activation and secretion of proinflammatory cytokines. After Nrf2 activation, the downstream antioxidant upregulation can act as a primary cellular defense against the cytotoxic effects of oxidative stress and help to promote hepatic recovery during IR. The complex crosstalk between Nrf2 and cellular pathways in liver IR injury and the potential therapeutic target of the Nrf2 inducers will be discussed in the present review.
Nrf2 activates different cellular mechanisms in response to ischemia‐reperfusion (IR) injury in liver. IR is a major cause of graft loss and dysfunction in clinical transplantation and organ resection. During the IR process, ROS generation leads oxidative stress, inflammation and mitochondrial dysfunction. After Nrf2 activation, the downstream antioxidant upregulation can act as a primary cellular defense and help to promote hepatic recovery during IR.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>34967991</pmid><doi>10.1111/febs.16336</doi><tpages>5479</tpages><orcidid>https://orcid.org/0000-0002-7131-3667</orcidid><orcidid>https://orcid.org/0000-0003-0645-6140</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Activating transcription factor 3 antioxidant Antioxidants Apoptosis Biomolecules Cell death Cytokines Cytotoxicity Detoxification Gene expression Gene regulation Hepatocytes Homeostasis Inflammasomes Inflammation Injuries Ischemia ischemia‐reperfusion injury Liver miRNA Mitochondria Nrf2 Oxidation Oxidative stress Reactive oxygen species redox Reperfusion Therapeutic targets Transcription Transplantation |
| title | Nrf2 and oxidative stress in liver ischemia/reperfusion injury |
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