A Mitochondria‐Targeted Ferroptosis Inducer Activated by Glutathione‐Responsive Imaging and Depletion for Triple Negative Breast Cancer Theranostics
Ferroptosis is a new type of iron‐dependent programmed cell death characterized by glutathione (GSH) depletion, selenoprotein glutathione peroxidase 4 (GPX4) inactivation, and lipid peroxides accumulation. Mitochondria, as the main source of intracellular energy supply and reactive oxygen species (R...
Gespeichert in:
| Veröffentlicht in: | Advanced healthcare materials 2023-09, Vol.12 (22), p.e2300220-n/a |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | n/a |
|---|---|
| container_issue | 22 |
| container_start_page | e2300220 |
| container_title | Advanced healthcare materials |
| container_volume | 12 |
| creator | Gan, Hongbo Huang, Xie Luo, Xi Li, Jinlin Mo, Banghui Cheng, Lizhi Shu, Qiuxia Du, Zaizhi Tang, Hong Sun, Wei Wang, Liting Luo, Shenglin Yu, Songtao |
| description | Ferroptosis is a new type of iron‐dependent programmed cell death characterized by glutathione (GSH) depletion, selenoprotein glutathione peroxidase 4 (GPX4) inactivation, and lipid peroxides accumulation. Mitochondria, as the main source of intracellular energy supply and reactive oxygen species (ROS) generation, play a central role in oxidative phosphorylation and redox homeostasis. Therefore, targeting cancer‐cell mitochondria and attacking redox homeostasis is expected to induce robust ferroptosis‐mediated anticancer effects. In this work, a theranostic ferroptosis inducer (IR780‐SPhF), which can simultaneously achieve the imaging and therapy of triple‐negative breast cancer (TNBC) by targeting mitochondria is presented. It is developed from a mitochondria‐targeting small molecule (IR780) with cancer‐preferential accumulation, enabling it to react with GSH by nucleophilic substitution, resulting in mitochondrial GSH depletion and redox imbalance. More interestingly, IR780‐SPhF exhibits GSH‐responsive near‐infrared fluorescence emission and photoacoustic imaging characteristics, further facilitating diagnosis and treatment with real‐time monitoring of TNBC with a highly elevated GSH level. Both in vitro and in vivo results demonstrate that IR780‐SPhF exhibits potent anticancer effect, which is significantly stronger than cyclophosphamide, a classic drug commonly recommended for TNBC patients in clinic. Hence, the reported mitochondria‐targeted ferroptosis inducer may represent a promising candidate and a prospective strategy for efficient cancer treatment.
A mitochondria‐targeted ferroptosis inducer (IR780‐SPhF) activated by glutathione‐responsive imaging and depletion is designed for triple negative breast cancer theranostics. Through preferential accumulation of cancer cells and mitochondria, efficient mitochondrial GSH depletion, GPX4 inactivation, and lipid peroxides accumulation, ferroptosis‐mediated cell death is boosted remarkably by IR780‐SPhF. |
| doi_str_mv | 10.1002/adhm.202300220 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2816757988</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2859608828</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3730-3b14e0a9ac955647b0e03a4d1453daa30456464f3c53efb3aa5d17ce302de98f3</originalsourceid><addsrcrecordid>eNqFkctqGzEUhofQkoQ02y6LoJtu7Ooy16XrNIkhFwjuejgjnbEVZqSppEnwro_QZZ-vT1INTl3oJtocnaPvfAj-JHnP6JxRyj-D2vZzTrmIDadHySlnFZ_xPKveHO4pPUnOvX-k8eQZy0t2nJyIgtOUp_Q0-bUgtzpYubVGOQ2_f_xcg9tgQEUu0Tk7BOu1JyujRomOLGTQTzC9Njty1Y0BwlZbg3HvAf1gjddPSFY9bLTZEDCKXODQYYgMaa0ja6djS-5wA2EivzgEH8gSzGRfb9GBsT5o6d8lb1voPJ6_1LPk2-XX9fJ6dnN_tVoubmZSFILORMNSpFCBrLIsT4uGIhWQKpZmQgEImsZpnrZCZgLbRgBkihUSBeUKq7IVZ8mnvXdw9vuIPtS99hK7Dgza0de8ZHmRFVVZRvTjf-ijHZ2Jv4tUVuW0LPlEzfeUdNZ7h209ON2D29WM1lNs9RRbfYgtLnx40Y5Nj-qA_w0pAtUeeNYd7l7R1YuL69t_8j_ZuKeT</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2859608828</pqid></control><display><type>article</type><title>A Mitochondria‐Targeted Ferroptosis Inducer Activated by Glutathione‐Responsive Imaging and Depletion for Triple Negative Breast Cancer Theranostics</title><source>Wiley Online Library Journals Frontfile Complete</source><creator>Gan, Hongbo ; Huang, Xie ; Luo, Xi ; Li, Jinlin ; Mo, Banghui ; Cheng, Lizhi ; Shu, Qiuxia ; Du, Zaizhi ; Tang, Hong ; Sun, Wei ; Wang, Liting ; Luo, Shenglin ; Yu, Songtao</creator><creatorcontrib>Gan, Hongbo ; Huang, Xie ; Luo, Xi ; Li, Jinlin ; Mo, Banghui ; Cheng, Lizhi ; Shu, Qiuxia ; Du, Zaizhi ; Tang, Hong ; Sun, Wei ; Wang, Liting ; Luo, Shenglin ; Yu, Songtao</creatorcontrib><description>Ferroptosis is a new type of iron‐dependent programmed cell death characterized by glutathione (GSH) depletion, selenoprotein glutathione peroxidase 4 (GPX4) inactivation, and lipid peroxides accumulation. Mitochondria, as the main source of intracellular energy supply and reactive oxygen species (ROS) generation, play a central role in oxidative phosphorylation and redox homeostasis. Therefore, targeting cancer‐cell mitochondria and attacking redox homeostasis is expected to induce robust ferroptosis‐mediated anticancer effects. In this work, a theranostic ferroptosis inducer (IR780‐SPhF), which can simultaneously achieve the imaging and therapy of triple‐negative breast cancer (TNBC) by targeting mitochondria is presented. It is developed from a mitochondria‐targeting small molecule (IR780) with cancer‐preferential accumulation, enabling it to react with GSH by nucleophilic substitution, resulting in mitochondrial GSH depletion and redox imbalance. More interestingly, IR780‐SPhF exhibits GSH‐responsive near‐infrared fluorescence emission and photoacoustic imaging characteristics, further facilitating diagnosis and treatment with real‐time monitoring of TNBC with a highly elevated GSH level. Both in vitro and in vivo results demonstrate that IR780‐SPhF exhibits potent anticancer effect, which is significantly stronger than cyclophosphamide, a classic drug commonly recommended for TNBC patients in clinic. Hence, the reported mitochondria‐targeted ferroptosis inducer may represent a promising candidate and a prospective strategy for efficient cancer treatment.
A mitochondria‐targeted ferroptosis inducer (IR780‐SPhF) activated by glutathione‐responsive imaging and depletion is designed for triple negative breast cancer theranostics. Through preferential accumulation of cancer cells and mitochondria, efficient mitochondrial GSH depletion, GPX4 inactivation, and lipid peroxides accumulation, ferroptosis‐mediated cell death is boosted remarkably by IR780‐SPhF.</description><identifier>ISSN: 2192-2640</identifier><identifier>EISSN: 2192-2659</identifier><identifier>DOI: 10.1002/adhm.202300220</identifier><identifier>PMID: 37204240</identifier><language>eng</language><publisher>Germany: Wiley Subscription Services, Inc</publisher><subject>Accumulation ; Anticancer properties ; Apoptosis ; Breast cancer ; Cancer therapies ; Cell death ; Cyclophosphamide ; Depletion ; Ferroptosis ; Glutathione ; Glutathione peroxidase ; heptamethine dyes ; Homeostasis ; Lipids ; Medical imaging ; Mitochondria ; Near infrared radiation ; Oxidative phosphorylation ; Peroxidase ; Peroxides ; Phosphorylation ; Precision medicine ; Reactive oxygen species ; theranostics</subject><ispartof>Advanced healthcare materials, 2023-09, Vol.12 (22), p.e2300220-n/a</ispartof><rights>2023 Wiley‐VCH GmbH</rights><rights>2023 Wiley-VCH GmbH.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3730-3b14e0a9ac955647b0e03a4d1453daa30456464f3c53efb3aa5d17ce302de98f3</citedby><cites>FETCH-LOGICAL-c3730-3b14e0a9ac955647b0e03a4d1453daa30456464f3c53efb3aa5d17ce302de98f3</cites><orcidid>0000-0002-0804-9891 ; 0000-0002-2804-9581</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fadhm.202300220$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fadhm.202300220$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37204240$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gan, Hongbo</creatorcontrib><creatorcontrib>Huang, Xie</creatorcontrib><creatorcontrib>Luo, Xi</creatorcontrib><creatorcontrib>Li, Jinlin</creatorcontrib><creatorcontrib>Mo, Banghui</creatorcontrib><creatorcontrib>Cheng, Lizhi</creatorcontrib><creatorcontrib>Shu, Qiuxia</creatorcontrib><creatorcontrib>Du, Zaizhi</creatorcontrib><creatorcontrib>Tang, Hong</creatorcontrib><creatorcontrib>Sun, Wei</creatorcontrib><creatorcontrib>Wang, Liting</creatorcontrib><creatorcontrib>Luo, Shenglin</creatorcontrib><creatorcontrib>Yu, Songtao</creatorcontrib><title>A Mitochondria‐Targeted Ferroptosis Inducer Activated by Glutathione‐Responsive Imaging and Depletion for Triple Negative Breast Cancer Theranostics</title><title>Advanced healthcare materials</title><addtitle>Adv Healthc Mater</addtitle><description>Ferroptosis is a new type of iron‐dependent programmed cell death characterized by glutathione (GSH) depletion, selenoprotein glutathione peroxidase 4 (GPX4) inactivation, and lipid peroxides accumulation. Mitochondria, as the main source of intracellular energy supply and reactive oxygen species (ROS) generation, play a central role in oxidative phosphorylation and redox homeostasis. Therefore, targeting cancer‐cell mitochondria and attacking redox homeostasis is expected to induce robust ferroptosis‐mediated anticancer effects. In this work, a theranostic ferroptosis inducer (IR780‐SPhF), which can simultaneously achieve the imaging and therapy of triple‐negative breast cancer (TNBC) by targeting mitochondria is presented. It is developed from a mitochondria‐targeting small molecule (IR780) with cancer‐preferential accumulation, enabling it to react with GSH by nucleophilic substitution, resulting in mitochondrial GSH depletion and redox imbalance. More interestingly, IR780‐SPhF exhibits GSH‐responsive near‐infrared fluorescence emission and photoacoustic imaging characteristics, further facilitating diagnosis and treatment with real‐time monitoring of TNBC with a highly elevated GSH level. Both in vitro and in vivo results demonstrate that IR780‐SPhF exhibits potent anticancer effect, which is significantly stronger than cyclophosphamide, a classic drug commonly recommended for TNBC patients in clinic. Hence, the reported mitochondria‐targeted ferroptosis inducer may represent a promising candidate and a prospective strategy for efficient cancer treatment.
A mitochondria‐targeted ferroptosis inducer (IR780‐SPhF) activated by glutathione‐responsive imaging and depletion is designed for triple negative breast cancer theranostics. Through preferential accumulation of cancer cells and mitochondria, efficient mitochondrial GSH depletion, GPX4 inactivation, and lipid peroxides accumulation, ferroptosis‐mediated cell death is boosted remarkably by IR780‐SPhF.</description><subject>Accumulation</subject><subject>Anticancer properties</subject><subject>Apoptosis</subject><subject>Breast cancer</subject><subject>Cancer therapies</subject><subject>Cell death</subject><subject>Cyclophosphamide</subject><subject>Depletion</subject><subject>Ferroptosis</subject><subject>Glutathione</subject><subject>Glutathione peroxidase</subject><subject>heptamethine dyes</subject><subject>Homeostasis</subject><subject>Lipids</subject><subject>Medical imaging</subject><subject>Mitochondria</subject><subject>Near infrared radiation</subject><subject>Oxidative phosphorylation</subject><subject>Peroxidase</subject><subject>Peroxides</subject><subject>Phosphorylation</subject><subject>Precision medicine</subject><subject>Reactive oxygen species</subject><subject>theranostics</subject><issn>2192-2640</issn><issn>2192-2659</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNqFkctqGzEUhofQkoQ02y6LoJtu7Ooy16XrNIkhFwjuejgjnbEVZqSppEnwro_QZZ-vT1INTl3oJtocnaPvfAj-JHnP6JxRyj-D2vZzTrmIDadHySlnFZ_xPKveHO4pPUnOvX-k8eQZy0t2nJyIgtOUp_Q0-bUgtzpYubVGOQ2_f_xcg9tgQEUu0Tk7BOu1JyujRomOLGTQTzC9Njty1Y0BwlZbg3HvAf1gjddPSFY9bLTZEDCKXODQYYgMaa0ja6djS-5wA2EivzgEH8gSzGRfb9GBsT5o6d8lb1voPJ6_1LPk2-XX9fJ6dnN_tVoubmZSFILORMNSpFCBrLIsT4uGIhWQKpZmQgEImsZpnrZCZgLbRgBkihUSBeUKq7IVZ8mnvXdw9vuIPtS99hK7Dgza0de8ZHmRFVVZRvTjf-ijHZ2Jv4tUVuW0LPlEzfeUdNZ7h209ON2D29WM1lNs9RRbfYgtLnx40Y5Nj-qA_w0pAtUeeNYd7l7R1YuL69t_8j_ZuKeT</recordid><startdate>20230901</startdate><enddate>20230901</enddate><creator>Gan, Hongbo</creator><creator>Huang, Xie</creator><creator>Luo, Xi</creator><creator>Li, Jinlin</creator><creator>Mo, Banghui</creator><creator>Cheng, Lizhi</creator><creator>Shu, Qiuxia</creator><creator>Du, Zaizhi</creator><creator>Tang, Hong</creator><creator>Sun, Wei</creator><creator>Wang, Liting</creator><creator>Luo, Shenglin</creator><creator>Yu, Songtao</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QF</scope><scope>7QP</scope><scope>7QQ</scope><scope>7SC</scope><scope>7SE</scope><scope>7SP</scope><scope>7SR</scope><scope>7T5</scope><scope>7TA</scope><scope>7TB</scope><scope>7TM</scope><scope>7TO</scope><scope>7U5</scope><scope>8BQ</scope><scope>8FD</scope><scope>F28</scope><scope>FR3</scope><scope>H8D</scope><scope>H8G</scope><scope>H94</scope><scope>JG9</scope><scope>JQ2</scope><scope>K9.</scope><scope>KR7</scope><scope>L7M</scope><scope>L~C</scope><scope>L~D</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-0804-9891</orcidid><orcidid>https://orcid.org/0000-0002-2804-9581</orcidid></search><sort><creationdate>20230901</creationdate><title>A Mitochondria‐Targeted Ferroptosis Inducer Activated by Glutathione‐Responsive Imaging and Depletion for Triple Negative Breast Cancer Theranostics</title><author>Gan, Hongbo ; Huang, Xie ; Luo, Xi ; Li, Jinlin ; Mo, Banghui ; Cheng, Lizhi ; Shu, Qiuxia ; Du, Zaizhi ; Tang, Hong ; Sun, Wei ; Wang, Liting ; Luo, Shenglin ; Yu, Songtao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3730-3b14e0a9ac955647b0e03a4d1453daa30456464f3c53efb3aa5d17ce302de98f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Accumulation</topic><topic>Anticancer properties</topic><topic>Apoptosis</topic><topic>Breast cancer</topic><topic>Cancer therapies</topic><topic>Cell death</topic><topic>Cyclophosphamide</topic><topic>Depletion</topic><topic>Ferroptosis</topic><topic>Glutathione</topic><topic>Glutathione peroxidase</topic><topic>heptamethine dyes</topic><topic>Homeostasis</topic><topic>Lipids</topic><topic>Medical imaging</topic><topic>Mitochondria</topic><topic>Near infrared radiation</topic><topic>Oxidative phosphorylation</topic><topic>Peroxidase</topic><topic>Peroxides</topic><topic>Phosphorylation</topic><topic>Precision medicine</topic><topic>Reactive oxygen species</topic><topic>theranostics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gan, Hongbo</creatorcontrib><creatorcontrib>Huang, Xie</creatorcontrib><creatorcontrib>Luo, Xi</creatorcontrib><creatorcontrib>Li, Jinlin</creatorcontrib><creatorcontrib>Mo, Banghui</creatorcontrib><creatorcontrib>Cheng, Lizhi</creatorcontrib><creatorcontrib>Shu, Qiuxia</creatorcontrib><creatorcontrib>Du, Zaizhi</creatorcontrib><creatorcontrib>Tang, Hong</creatorcontrib><creatorcontrib>Sun, Wei</creatorcontrib><creatorcontrib>Wang, Liting</creatorcontrib><creatorcontrib>Luo, Shenglin</creatorcontrib><creatorcontrib>Yu, Songtao</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Aluminium Industry Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Ceramic Abstracts</collection><collection>Computer and Information Systems Abstracts</collection><collection>Corrosion Abstracts</collection><collection>Electronics & Communications Abstracts</collection><collection>Engineered Materials Abstracts</collection><collection>Immunology Abstracts</collection><collection>Materials Business File</collection><collection>Mechanical & Transportation Engineering Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>METADEX</collection><collection>Technology Research Database</collection><collection>ANTE: Abstracts in New Technology & Engineering</collection><collection>Engineering Research Database</collection><collection>Aerospace Database</collection><collection>Copper Technical Reference Library</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Materials Research Database</collection><collection>ProQuest Computer Science Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Civil Engineering Abstracts</collection><collection>Advanced Technologies Database with Aerospace</collection><collection>Computer and Information Systems Abstracts Academic</collection><collection>Computer and Information Systems Abstracts Professional</collection><collection>MEDLINE - Academic</collection><jtitle>Advanced healthcare materials</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gan, Hongbo</au><au>Huang, Xie</au><au>Luo, Xi</au><au>Li, Jinlin</au><au>Mo, Banghui</au><au>Cheng, Lizhi</au><au>Shu, Qiuxia</au><au>Du, Zaizhi</au><au>Tang, Hong</au><au>Sun, Wei</au><au>Wang, Liting</au><au>Luo, Shenglin</au><au>Yu, Songtao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Mitochondria‐Targeted Ferroptosis Inducer Activated by Glutathione‐Responsive Imaging and Depletion for Triple Negative Breast Cancer Theranostics</atitle><jtitle>Advanced healthcare materials</jtitle><addtitle>Adv Healthc Mater</addtitle><date>2023-09-01</date><risdate>2023</risdate><volume>12</volume><issue>22</issue><spage>e2300220</spage><epage>n/a</epage><pages>e2300220-n/a</pages><issn>2192-2640</issn><eissn>2192-2659</eissn><abstract>Ferroptosis is a new type of iron‐dependent programmed cell death characterized by glutathione (GSH) depletion, selenoprotein glutathione peroxidase 4 (GPX4) inactivation, and lipid peroxides accumulation. Mitochondria, as the main source of intracellular energy supply and reactive oxygen species (ROS) generation, play a central role in oxidative phosphorylation and redox homeostasis. Therefore, targeting cancer‐cell mitochondria and attacking redox homeostasis is expected to induce robust ferroptosis‐mediated anticancer effects. In this work, a theranostic ferroptosis inducer (IR780‐SPhF), which can simultaneously achieve the imaging and therapy of triple‐negative breast cancer (TNBC) by targeting mitochondria is presented. It is developed from a mitochondria‐targeting small molecule (IR780) with cancer‐preferential accumulation, enabling it to react with GSH by nucleophilic substitution, resulting in mitochondrial GSH depletion and redox imbalance. More interestingly, IR780‐SPhF exhibits GSH‐responsive near‐infrared fluorescence emission and photoacoustic imaging characteristics, further facilitating diagnosis and treatment with real‐time monitoring of TNBC with a highly elevated GSH level. Both in vitro and in vivo results demonstrate that IR780‐SPhF exhibits potent anticancer effect, which is significantly stronger than cyclophosphamide, a classic drug commonly recommended for TNBC patients in clinic. Hence, the reported mitochondria‐targeted ferroptosis inducer may represent a promising candidate and a prospective strategy for efficient cancer treatment.
A mitochondria‐targeted ferroptosis inducer (IR780‐SPhF) activated by glutathione‐responsive imaging and depletion is designed for triple negative breast cancer theranostics. Through preferential accumulation of cancer cells and mitochondria, efficient mitochondrial GSH depletion, GPX4 inactivation, and lipid peroxides accumulation, ferroptosis‐mediated cell death is boosted remarkably by IR780‐SPhF.</abstract><cop>Germany</cop><pub>Wiley Subscription Services, Inc</pub><pmid>37204240</pmid><doi>10.1002/adhm.202300220</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-0804-9891</orcidid><orcidid>https://orcid.org/0000-0002-2804-9581</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2192-2640 |
| ispartof | Advanced healthcare materials, 2023-09, Vol.12 (22), p.e2300220-n/a |
| issn | 2192-2640 2192-2659 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2816757988 |
| source | Wiley Online Library Journals Frontfile Complete |
| subjects | Accumulation Anticancer properties Apoptosis Breast cancer Cancer therapies Cell death Cyclophosphamide Depletion Ferroptosis Glutathione Glutathione peroxidase heptamethine dyes Homeostasis Lipids Medical imaging Mitochondria Near infrared radiation Oxidative phosphorylation Peroxidase Peroxides Phosphorylation Precision medicine Reactive oxygen species theranostics |
| title | A Mitochondria‐Targeted Ferroptosis Inducer Activated by Glutathione‐Responsive Imaging and Depletion for Triple Negative Breast Cancer Theranostics |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T18%3A38%3A56IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=A%20Mitochondria%E2%80%90Targeted%20Ferroptosis%20Inducer%20Activated%20by%20Glutathione%E2%80%90Responsive%20Imaging%20and%20Depletion%20for%20Triple%20Negative%20Breast%20Cancer%20Theranostics&rft.jtitle=Advanced%20healthcare%20materials&rft.au=Gan,%20Hongbo&rft.date=2023-09-01&rft.volume=12&rft.issue=22&rft.spage=e2300220&rft.epage=n/a&rft.pages=e2300220-n/a&rft.issn=2192-2640&rft.eissn=2192-2659&rft_id=info:doi/10.1002/adhm.202300220&rft_dat=%3Cproquest_cross%3E2859608828%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2859608828&rft_id=info:pmid/37204240&rfr_iscdi=true |