Doxorubicin‐induced cardiotoxicity involves IFNγ‐mediated metabolic reprogramming in cardiomyocytes
Immune responses contribute to a large extent to heart diseases. However, it is still not clear how the key inflammatory mediator interferon‐γ (IFNγ) plays a role in doxorubicin (DOX)‐induced cardiomyopathy. We report here that DOX‐induced heart dysfunction involves IFNγ signaling in mice. The IFNγ...
Gespeichert in:
| Veröffentlicht in: | The Journal of pathology 2019-03, Vol.247 (3), p.320-332 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 332 |
|---|---|
| container_issue | 3 |
| container_start_page | 320 |
| container_title | The Journal of pathology |
| container_volume | 247 |
| creator | Ni, Chen Ma, Pan Wang, Ruirui Lou, Xiaohan Liu, Xiaomeng Qin, Yue Xue, Rui Blasig, Ingolf Erben, Ulrike Qin, Zhihai |
| description | Immune responses contribute to a large extent to heart diseases. However, it is still not clear how the key inflammatory mediator interferon‐γ (IFNγ) plays a role in doxorubicin (DOX)‐induced cardiomyopathy. We report here that DOX‐induced heart dysfunction involves IFNγ signaling in mice. The IFNγ receptor was found to be highly expressed on cardiomyocytes, and its downstream signaling was activated in heart tissues upon DOX treatment. In vitro, IFNγ strongly aggravated the injury of cardiomyocytes exposed to DOX. Although not affecting DOX‐induced cell death, IFNγ disrupted mitochondrial respiration and fatty acid oxidation in DOX‐exposed cardiomyocytes. IFNγ extended the suppression of the AMP‐activated protein kinase (AMPK)/acetyl‐CoA carboxylase (ACC) axis by DOX to a p38‐dependent branch. Activation of AMPK or inhibition of p38 inhibited the enhancing effect of IFNγ on the DOX‐induced cardiotoxicity and prolonged the survival time in DOX‐treated mice. Taken together, our results indicate that reprogramming of cardiac metabolism by IFNγ represents a previously unidentified key step for DOX‐induced cardiomyopathy. This unavoidable impact of IFNγ on cardiomyocyte metabolism during chemotherapy redirects our attention to the balance between beneficial immunosurveillance of cancer cells and unwanted toxic side‐effects. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. |
| doi_str_mv | 10.1002/path.5192 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2177547430</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2177547430</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3532-63f4104daf780fd2c6a4ceb25983af40307f49d0117f3710505fe3cb319d92993</originalsourceid><addsrcrecordid>eNp1kEtOwzAURS0EgvIZsAFUiRGDlOdPknqIgNJKFTAo48hxbDBK4mInpZmxBPbCPlgEK8GlhRmjJ_kdH_tehI4xDDAAOZ-L5mkQY062UA8DTyI-5Mk26oUdiSjD6R7a9_4ZADiP4120R4GRJIa4h56u7NK6NjfS1F9v76YuWqmKvhSuMLaxy3DedH1TL2y5UL4_Gd1-fgSuUoURTQAr1Yjclkb2nZo7--hEVZn6MdzYOKrOyq5R_hDtaFF6dbSZB-hhdD27HEfTu5vJ5cU0kjSmJEqoZhhYIXQ6BF0QmQgmVU5iPqRCM6CQasYLwDjVNMUQQmhFZU4xLzjhnB6g07U3_OalVb7Jnm3r6vBkRnCaxixlFAJ1tqaks947pbO5M5VwXYYhW3WarTrNVp0G9mRjbPOQ-4_8LTEA52vg1ZSq-9-U3V_Mxj_KbxnMhTc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2177547430</pqid></control><display><type>article</type><title>Doxorubicin‐induced cardiotoxicity involves IFNγ‐mediated metabolic reprogramming in cardiomyocytes</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Ni, Chen ; Ma, Pan ; Wang, Ruirui ; Lou, Xiaohan ; Liu, Xiaomeng ; Qin, Yue ; Xue, Rui ; Blasig, Ingolf ; Erben, Ulrike ; Qin, Zhihai</creator><creatorcontrib>Ni, Chen ; Ma, Pan ; Wang, Ruirui ; Lou, Xiaohan ; Liu, Xiaomeng ; Qin, Yue ; Xue, Rui ; Blasig, Ingolf ; Erben, Ulrike ; Qin, Zhihai</creatorcontrib><description>Immune responses contribute to a large extent to heart diseases. However, it is still not clear how the key inflammatory mediator interferon‐γ (IFNγ) plays a role in doxorubicin (DOX)‐induced cardiomyopathy. We report here that DOX‐induced heart dysfunction involves IFNγ signaling in mice. The IFNγ receptor was found to be highly expressed on cardiomyocytes, and its downstream signaling was activated in heart tissues upon DOX treatment. In vitro, IFNγ strongly aggravated the injury of cardiomyocytes exposed to DOX. Although not affecting DOX‐induced cell death, IFNγ disrupted mitochondrial respiration and fatty acid oxidation in DOX‐exposed cardiomyocytes. IFNγ extended the suppression of the AMP‐activated protein kinase (AMPK)/acetyl‐CoA carboxylase (ACC) axis by DOX to a p38‐dependent branch. Activation of AMPK or inhibition of p38 inhibited the enhancing effect of IFNγ on the DOX‐induced cardiotoxicity and prolonged the survival time in DOX‐treated mice. Taken together, our results indicate that reprogramming of cardiac metabolism by IFNγ represents a previously unidentified key step for DOX‐induced cardiomyopathy. This unavoidable impact of IFNγ on cardiomyocyte metabolism during chemotherapy redirects our attention to the balance between beneficial immunosurveillance of cancer cells and unwanted toxic side‐effects. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</description><identifier>ISSN: 0022-3417</identifier><identifier>EISSN: 1096-9896</identifier><identifier>DOI: 10.1002/path.5192</identifier><identifier>PMID: 30426505</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>AMP ; Animals ; Antibiotics, Antineoplastic - pharmacology ; Antibiotics, Antineoplastic - toxicity ; Cancer ; Cardiomyocytes ; Cardiomyopathy ; Cardiotoxicity ; Cardiotoxicity - etiology ; Cardiotoxicity - immunology ; Cardiotoxicity - pathology ; Cardiovascular diseases ; Cell death ; Cell Respiration - physiology ; Cells, Cultured ; Cellular Reprogramming - drug effects ; Cellular Reprogramming - immunology ; Chemotherapy ; Coronary artery disease ; Doxorubicin ; Doxorubicin - pharmacology ; Doxorubicin - toxicity ; Electron transport ; fatty acid metabolism ; Fatty Acids - metabolism ; Female ; Heart diseases ; IFNγ ; Immune response ; Immunosurveillance ; Inflammation ; Interferon ; Interferon-gamma - immunology ; Kinases ; Metabolism ; Mice ; Mice, Inbred C57BL ; Mitochondria ; Mitochondria, Heart - metabolism ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - immunology ; Oxidation ; Oxidation-Reduction ; Protein kinase ; Receptor, Interferon alpha-beta - metabolism ; Signal Transduction - immunology ; γ-Interferon</subject><ispartof>The Journal of pathology, 2019-03, Vol.247 (3), p.320-332</ispartof><rights>Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</rights><rights>Copyright © 2019 Pathological Society of Great Britain and Ireland</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3532-63f4104daf780fd2c6a4ceb25983af40307f49d0117f3710505fe3cb319d92993</citedby><cites>FETCH-LOGICAL-c3532-63f4104daf780fd2c6a4ceb25983af40307f49d0117f3710505fe3cb319d92993</cites><orcidid>0000-0001-9793-7964 ; 0000-0002-7993-8055</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%2Fpath.5192$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fpath.5192$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30426505$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ni, Chen</creatorcontrib><creatorcontrib>Ma, Pan</creatorcontrib><creatorcontrib>Wang, Ruirui</creatorcontrib><creatorcontrib>Lou, Xiaohan</creatorcontrib><creatorcontrib>Liu, Xiaomeng</creatorcontrib><creatorcontrib>Qin, Yue</creatorcontrib><creatorcontrib>Xue, Rui</creatorcontrib><creatorcontrib>Blasig, Ingolf</creatorcontrib><creatorcontrib>Erben, Ulrike</creatorcontrib><creatorcontrib>Qin, Zhihai</creatorcontrib><title>Doxorubicin‐induced cardiotoxicity involves IFNγ‐mediated metabolic reprogramming in cardiomyocytes</title><title>The Journal of pathology</title><addtitle>J Pathol</addtitle><description>Immune responses contribute to a large extent to heart diseases. However, it is still not clear how the key inflammatory mediator interferon‐γ (IFNγ) plays a role in doxorubicin (DOX)‐induced cardiomyopathy. We report here that DOX‐induced heart dysfunction involves IFNγ signaling in mice. The IFNγ receptor was found to be highly expressed on cardiomyocytes, and its downstream signaling was activated in heart tissues upon DOX treatment. In vitro, IFNγ strongly aggravated the injury of cardiomyocytes exposed to DOX. Although not affecting DOX‐induced cell death, IFNγ disrupted mitochondrial respiration and fatty acid oxidation in DOX‐exposed cardiomyocytes. IFNγ extended the suppression of the AMP‐activated protein kinase (AMPK)/acetyl‐CoA carboxylase (ACC) axis by DOX to a p38‐dependent branch. Activation of AMPK or inhibition of p38 inhibited the enhancing effect of IFNγ on the DOX‐induced cardiotoxicity and prolonged the survival time in DOX‐treated mice. Taken together, our results indicate that reprogramming of cardiac metabolism by IFNγ represents a previously unidentified key step for DOX‐induced cardiomyopathy. This unavoidable impact of IFNγ on cardiomyocyte metabolism during chemotherapy redirects our attention to the balance between beneficial immunosurveillance of cancer cells and unwanted toxic side‐effects. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</description><subject>AMP</subject><subject>Animals</subject><subject>Antibiotics, Antineoplastic - pharmacology</subject><subject>Antibiotics, Antineoplastic - toxicity</subject><subject>Cancer</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathy</subject><subject>Cardiotoxicity</subject><subject>Cardiotoxicity - etiology</subject><subject>Cardiotoxicity - immunology</subject><subject>Cardiotoxicity - pathology</subject><subject>Cardiovascular diseases</subject><subject>Cell death</subject><subject>Cell Respiration - physiology</subject><subject>Cells, Cultured</subject><subject>Cellular Reprogramming - drug effects</subject><subject>Cellular Reprogramming - immunology</subject><subject>Chemotherapy</subject><subject>Coronary artery disease</subject><subject>Doxorubicin</subject><subject>Doxorubicin - pharmacology</subject><subject>Doxorubicin - toxicity</subject><subject>Electron transport</subject><subject>fatty acid metabolism</subject><subject>Fatty Acids - metabolism</subject><subject>Female</subject><subject>Heart diseases</subject><subject>IFNγ</subject><subject>Immune response</subject><subject>Immunosurveillance</subject><subject>Inflammation</subject><subject>Interferon</subject><subject>Interferon-gamma - immunology</subject><subject>Kinases</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mitochondria</subject><subject>Mitochondria, Heart - metabolism</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - immunology</subject><subject>Oxidation</subject><subject>Oxidation-Reduction</subject><subject>Protein kinase</subject><subject>Receptor, Interferon alpha-beta - metabolism</subject><subject>Signal Transduction - immunology</subject><subject>γ-Interferon</subject><issn>0022-3417</issn><issn>1096-9896</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEtOwzAURS0EgvIZsAFUiRGDlOdPknqIgNJKFTAo48hxbDBK4mInpZmxBPbCPlgEK8GlhRmjJ_kdH_tehI4xDDAAOZ-L5mkQY062UA8DTyI-5Mk26oUdiSjD6R7a9_4ZADiP4120R4GRJIa4h56u7NK6NjfS1F9v76YuWqmKvhSuMLaxy3DedH1TL2y5UL4_Gd1-fgSuUoURTQAr1Yjclkb2nZo7--hEVZn6MdzYOKrOyq5R_hDtaFF6dbSZB-hhdD27HEfTu5vJ5cU0kjSmJEqoZhhYIXQ6BF0QmQgmVU5iPqRCM6CQasYLwDjVNMUQQmhFZU4xLzjhnB6g07U3_OalVb7Jnm3r6vBkRnCaxixlFAJ1tqaks947pbO5M5VwXYYhW3WarTrNVp0G9mRjbPOQ-4_8LTEA52vg1ZSq-9-U3V_Mxj_KbxnMhTc</recordid><startdate>201903</startdate><enddate>201903</enddate><creator>Ni, Chen</creator><creator>Ma, Pan</creator><creator>Wang, Ruirui</creator><creator>Lou, Xiaohan</creator><creator>Liu, Xiaomeng</creator><creator>Qin, Yue</creator><creator>Xue, Rui</creator><creator>Blasig, Ingolf</creator><creator>Erben, Ulrike</creator><creator>Qin, Zhihai</creator><general>John Wiley & Sons, Ltd</general><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><orcidid>https://orcid.org/0000-0001-9793-7964</orcidid><orcidid>https://orcid.org/0000-0002-7993-8055</orcidid></search><sort><creationdate>201903</creationdate><title>Doxorubicin‐induced cardiotoxicity involves IFNγ‐mediated metabolic reprogramming in cardiomyocytes</title><author>Ni, Chen ; Ma, Pan ; Wang, Ruirui ; Lou, Xiaohan ; Liu, Xiaomeng ; Qin, Yue ; Xue, Rui ; Blasig, Ingolf ; Erben, Ulrike ; Qin, Zhihai</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3532-63f4104daf780fd2c6a4ceb25983af40307f49d0117f3710505fe3cb319d92993</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>AMP</topic><topic>Animals</topic><topic>Antibiotics, Antineoplastic - pharmacology</topic><topic>Antibiotics, Antineoplastic - toxicity</topic><topic>Cancer</topic><topic>Cardiomyocytes</topic><topic>Cardiomyopathy</topic><topic>Cardiotoxicity</topic><topic>Cardiotoxicity - etiology</topic><topic>Cardiotoxicity - immunology</topic><topic>Cardiotoxicity - pathology</topic><topic>Cardiovascular diseases</topic><topic>Cell death</topic><topic>Cell Respiration - physiology</topic><topic>Cells, Cultured</topic><topic>Cellular Reprogramming - drug effects</topic><topic>Cellular Reprogramming - immunology</topic><topic>Chemotherapy</topic><topic>Coronary artery disease</topic><topic>Doxorubicin</topic><topic>Doxorubicin - pharmacology</topic><topic>Doxorubicin - toxicity</topic><topic>Electron transport</topic><topic>fatty acid metabolism</topic><topic>Fatty Acids - metabolism</topic><topic>Female</topic><topic>Heart diseases</topic><topic>IFNγ</topic><topic>Immune response</topic><topic>Immunosurveillance</topic><topic>Inflammation</topic><topic>Interferon</topic><topic>Interferon-gamma - immunology</topic><topic>Kinases</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mitochondria</topic><topic>Mitochondria, Heart - metabolism</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - immunology</topic><topic>Oxidation</topic><topic>Oxidation-Reduction</topic><topic>Protein kinase</topic><topic>Receptor, Interferon alpha-beta - metabolism</topic><topic>Signal Transduction - immunology</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ni, Chen</creatorcontrib><creatorcontrib>Ma, Pan</creatorcontrib><creatorcontrib>Wang, Ruirui</creatorcontrib><creatorcontrib>Lou, Xiaohan</creatorcontrib><creatorcontrib>Liu, Xiaomeng</creatorcontrib><creatorcontrib>Qin, Yue</creatorcontrib><creatorcontrib>Xue, Rui</creatorcontrib><creatorcontrib>Blasig, Ingolf</creatorcontrib><creatorcontrib>Erben, Ulrike</creatorcontrib><creatorcontrib>Qin, Zhihai</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>The Journal of pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ni, Chen</au><au>Ma, Pan</au><au>Wang, Ruirui</au><au>Lou, Xiaohan</au><au>Liu, Xiaomeng</au><au>Qin, Yue</au><au>Xue, Rui</au><au>Blasig, Ingolf</au><au>Erben, Ulrike</au><au>Qin, Zhihai</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Doxorubicin‐induced cardiotoxicity involves IFNγ‐mediated metabolic reprogramming in cardiomyocytes</atitle><jtitle>The Journal of pathology</jtitle><addtitle>J Pathol</addtitle><date>2019-03</date><risdate>2019</risdate><volume>247</volume><issue>3</issue><spage>320</spage><epage>332</epage><pages>320-332</pages><issn>0022-3417</issn><eissn>1096-9896</eissn><abstract>Immune responses contribute to a large extent to heart diseases. However, it is still not clear how the key inflammatory mediator interferon‐γ (IFNγ) plays a role in doxorubicin (DOX)‐induced cardiomyopathy. We report here that DOX‐induced heart dysfunction involves IFNγ signaling in mice. The IFNγ receptor was found to be highly expressed on cardiomyocytes, and its downstream signaling was activated in heart tissues upon DOX treatment. In vitro, IFNγ strongly aggravated the injury of cardiomyocytes exposed to DOX. Although not affecting DOX‐induced cell death, IFNγ disrupted mitochondrial respiration and fatty acid oxidation in DOX‐exposed cardiomyocytes. IFNγ extended the suppression of the AMP‐activated protein kinase (AMPK)/acetyl‐CoA carboxylase (ACC) axis by DOX to a p38‐dependent branch. Activation of AMPK or inhibition of p38 inhibited the enhancing effect of IFNγ on the DOX‐induced cardiotoxicity and prolonged the survival time in DOX‐treated mice. Taken together, our results indicate that reprogramming of cardiac metabolism by IFNγ represents a previously unidentified key step for DOX‐induced cardiomyopathy. This unavoidable impact of IFNγ on cardiomyocyte metabolism during chemotherapy redirects our attention to the balance between beneficial immunosurveillance of cancer cells and unwanted toxic side‐effects. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>30426505</pmid><doi>10.1002/path.5192</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-9793-7964</orcidid><orcidid>https://orcid.org/0000-0002-7993-8055</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0022-3417 |
| ispartof | The Journal of pathology, 2019-03, Vol.247 (3), p.320-332 |
| issn | 0022-3417 1096-9896 |
| language | eng |
| recordid | cdi_proquest_journals_2177547430 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | AMP Animals Antibiotics, Antineoplastic - pharmacology Antibiotics, Antineoplastic - toxicity Cancer Cardiomyocytes Cardiomyopathy Cardiotoxicity Cardiotoxicity - etiology Cardiotoxicity - immunology Cardiotoxicity - pathology Cardiovascular diseases Cell death Cell Respiration - physiology Cells, Cultured Cellular Reprogramming - drug effects Cellular Reprogramming - immunology Chemotherapy Coronary artery disease Doxorubicin Doxorubicin - pharmacology Doxorubicin - toxicity Electron transport fatty acid metabolism Fatty Acids - metabolism Female Heart diseases IFNγ Immune response Immunosurveillance Inflammation Interferon Interferon-gamma - immunology Kinases Metabolism Mice Mice, Inbred C57BL Mitochondria Mitochondria, Heart - metabolism Myocytes, Cardiac - drug effects Myocytes, Cardiac - immunology Oxidation Oxidation-Reduction Protein kinase Receptor, Interferon alpha-beta - metabolism Signal Transduction - immunology γ-Interferon |
| title | Doxorubicin‐induced cardiotoxicity involves IFNγ‐mediated metabolic reprogramming in cardiomyocytes |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-03T20%3A07%3A58IST&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=Doxorubicin%E2%80%90induced%20cardiotoxicity%20involves%20IFN%CE%B3%E2%80%90mediated%20metabolic%20reprogramming%20in%20cardiomyocytes&rft.jtitle=The%20Journal%20of%20pathology&rft.au=Ni,%20Chen&rft.date=2019-03&rft.volume=247&rft.issue=3&rft.spage=320&rft.epage=332&rft.pages=320-332&rft.issn=0022-3417&rft.eissn=1096-9896&rft_id=info:doi/10.1002/path.5192&rft_dat=%3Cproquest_cross%3E2177547430%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=2177547430&rft_id=info:pmid/30426505&rfr_iscdi=true |