The Mechanisms of Ferroptosis Under Hypoxia
Ferroptosis is a new form of programmed cell death, which is characterized by the iron-dependent accumulation of lipid peroxidation and increase of ROS, resulting in oxidative stress and cell death. Iron, lipid, and multiple signaling pathways precisely control the occurrence and implementation of f...
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| Veröffentlicht in: | Cellular and molecular neurobiology 2023-10, Vol.43 (7), p.3329-3341 |
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| container_title | Cellular and molecular neurobiology |
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| creator | Gao, Xin Hu, Wei Qian, Dianlun Bai, Xiangfeng He, Huilin Li, Lin Sun, Shibo |
| description | Ferroptosis is a new form of programmed cell death, which is characterized by the iron-dependent accumulation of lipid peroxidation and increase of ROS, resulting in oxidative stress and cell death. Iron, lipid, and multiple signaling pathways precisely control the occurrence and implementation of ferroptosis. The pathways mainly include Nrf2/HO-1 signaling pathway, p62/Keap1/Nrf2 signaling pathway. Activating p62/Keap1/Nrf2 signaling pathway inhibits ferroptosis. Nrf2/HO-1 signaling pathway promotes ferroptosis. Furthermore, some factors also participate in the occurrence of ferroptosis under hypoxia, such as HIF-1, NCOA4, DMT1. Meanwhile, ferroptosis is related with hypoxia-related diseases, such as MIRI, cancers, and AKI. Accordingly, ferroptosis appears to be a therapeutic target for hypoxia-related diseases. |
| doi_str_mv | 10.1007/s10571-023-01388-8 |
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Iron, lipid, and multiple signaling pathways precisely control the occurrence and implementation of ferroptosis. The pathways mainly include Nrf2/HO-1 signaling pathway, p62/Keap1/Nrf2 signaling pathway. Activating p62/Keap1/Nrf2 signaling pathway inhibits ferroptosis. Nrf2/HO-1 signaling pathway promotes ferroptosis. Furthermore, some factors also participate in the occurrence of ferroptosis under hypoxia, such as HIF-1, NCOA4, DMT1. Meanwhile, ferroptosis is related with hypoxia-related diseases, such as MIRI, cancers, and AKI. Accordingly, ferroptosis appears to be a therapeutic target for hypoxia-related diseases.</description><identifier>ISSN: 0272-4340</identifier><identifier>EISSN: 1573-6830</identifier><identifier>DOI: 10.1007/s10571-023-01388-8</identifier><identifier>PMID: 37458878</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cell death ; Divalent metal transporter-1 ; Ferroptosis ; Hypoxia-inducible factor 1 ; Lipid peroxidation ; Neurobiology ; Neurosciences ; Oxidative stress ; Review Paper ; Signal transduction ; Therapeutic targets</subject><ispartof>Cellular and molecular neurobiology, 2023-10, Vol.43 (7), p.3329-3341</ispartof><rights>The Author(s) 2023</rights><rights>2023. The Author(s).</rights><rights>The Author(s) 2023. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). 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Iron, lipid, and multiple signaling pathways precisely control the occurrence and implementation of ferroptosis. The pathways mainly include Nrf2/HO-1 signaling pathway, p62/Keap1/Nrf2 signaling pathway. Activating p62/Keap1/Nrf2 signaling pathway inhibits ferroptosis. Nrf2/HO-1 signaling pathway promotes ferroptosis. Furthermore, some factors also participate in the occurrence of ferroptosis under hypoxia, such as HIF-1, NCOA4, DMT1. Meanwhile, ferroptosis is related with hypoxia-related diseases, such as MIRI, cancers, and AKI. Accordingly, ferroptosis appears to be a therapeutic target for hypoxia-related diseases.</description><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cell death</subject><subject>Divalent metal transporter-1</subject><subject>Ferroptosis</subject><subject>Hypoxia-inducible factor 1</subject><subject>Lipid peroxidation</subject><subject>Neurobiology</subject><subject>Neurosciences</subject><subject>Oxidative stress</subject><subject>Review Paper</subject><subject>Signal transduction</subject><subject>Therapeutic targets</subject><issn>0272-4340</issn><issn>1573-6830</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><recordid>eNp9kctOwzAQRS0EoqXwAyxQJDZIKDB-OyuEEC8JxKasLSeZtKnauNgtgr_H0PJcsJrFnLkzdy4h-xROKIA-jRSkpjkwngPlxuRmg_Sp1DxXhsMm6QPTLBdcQI_sxDgBgAJAbpMe10Iao02fHA_HmN1jNXZdG2cx8012hSH4-cLHNmaPXY0hu3md-5fW7ZKtxk0j7q3rgDxeXQ4vbvK7h-vbi_O7vBJaLnLBSiXA1VQBMsEc8kI2JXOFlrIEaaTEWkqDzFHOoKgaLpxgrEJnaqHrkg_I2Up3vixnWFfYLYKb2nloZy68Wu9a-7vTtWM78s-WgtCaKpUUjtYKwT8tMS7srI0VTqeuQ7-MlhleMKGUEgk9_INO_DJ0yV-iFGhhTEETxVZUFXyMAZuvayjY9zDsKgybwrAfYViThg5--vga-fx-AvgKiKnVjTB87_5H9g3BMpOW</recordid><startdate>20231001</startdate><enddate>20231001</enddate><creator>Gao, Xin</creator><creator>Hu, Wei</creator><creator>Qian, Dianlun</creator><creator>Bai, Xiangfeng</creator><creator>He, Huilin</creator><creator>Li, Lin</creator><creator>Sun, Shibo</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9287-1820</orcidid></search><sort><creationdate>20231001</creationdate><title>The Mechanisms of Ferroptosis Under Hypoxia</title><author>Gao, Xin ; Hu, Wei ; Qian, Dianlun ; Bai, Xiangfeng ; He, Huilin ; Li, Lin ; Sun, Shibo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c475t-42b640ad160e242ae395fb2a9755b05855ed558e2a13209cf34a422cea8d47db3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cell death</topic><topic>Divalent metal transporter-1</topic><topic>Ferroptosis</topic><topic>Hypoxia-inducible factor 1</topic><topic>Lipid peroxidation</topic><topic>Neurobiology</topic><topic>Neurosciences</topic><topic>Oxidative stress</topic><topic>Review Paper</topic><topic>Signal transduction</topic><topic>Therapeutic targets</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gao, Xin</creatorcontrib><creatorcontrib>Hu, Wei</creatorcontrib><creatorcontrib>Qian, Dianlun</creatorcontrib><creatorcontrib>Bai, Xiangfeng</creatorcontrib><creatorcontrib>He, Huilin</creatorcontrib><creatorcontrib>Li, Lin</creatorcontrib><creatorcontrib>Sun, Shibo</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cellular and molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gao, Xin</au><au>Hu, Wei</au><au>Qian, Dianlun</au><au>Bai, Xiangfeng</au><au>He, Huilin</au><au>Li, Lin</au><au>Sun, Shibo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Mechanisms of Ferroptosis Under Hypoxia</atitle><jtitle>Cellular and molecular neurobiology</jtitle><stitle>Cell Mol Neurobiol</stitle><addtitle>Cell Mol Neurobiol</addtitle><date>2023-10-01</date><risdate>2023</risdate><volume>43</volume><issue>7</issue><spage>3329</spage><epage>3341</epage><pages>3329-3341</pages><issn>0272-4340</issn><eissn>1573-6830</eissn><abstract>Ferroptosis is a new form of programmed cell death, which is characterized by the iron-dependent accumulation of lipid peroxidation and increase of ROS, resulting in oxidative stress and cell death. 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| subjects | Apoptosis Biomedical and Life Sciences Biomedicine Cell Biology Cell death Divalent metal transporter-1 Ferroptosis Hypoxia-inducible factor 1 Lipid peroxidation Neurobiology Neurosciences Oxidative stress Review Paper Signal transduction Therapeutic targets |
| title | The Mechanisms of Ferroptosis Under Hypoxia |
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