Targeting the Ferroptosis and Endoplasmic Reticulum Stress Signaling Pathways by CBX7 in Myocardial Ischemia/reperfusion Injury
Ferroptosis and endoplasmic reticulum stress (ERS) are common events in the process of myocardial ischemia/reperfusion injury (IRI). The suppression of chromobox7 (CBX7) has been reported to protect against ischemia/reperfusion injury, This research is purposed to expose the impacts and mechanism of...
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| container_title | Cell biochemistry and biophysics |
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| creator | Jiang, Weipeng Yan, Zeyu Zheng, Xueou Huang, Shiyi Hu, Yue Xiong, Fengjuan He, Bufan Wu, Yingzhi Fu, Qiang Li, Zhiliang Zhou, Baihua |
| description | Ferroptosis and endoplasmic reticulum stress (ERS) are common events in the process of myocardial ischemia/reperfusion injury (IRI). The suppression of chromobox7 (CBX7) has been reported to protect against ischemia/reperfusion injury, This research is purposed to expose the impacts and mechanism of CBX7 in myocardial IRI. CBX7 expression was detected using RT-qPCR and western blotting analysis. CCK-8 assay detected cell viability. Inflammatory response and oxidative stress were detected by ELISA, DCFH-DA probe and related assay kits. Flow cytometry analysis and caspase3 activity assay were used to detect cell apoptosis. C11-BODIPY 581/591 staining and ferro-orange staining were used to detect lipid reactive oxygen species (ROS) and Fe
2+
level, respectively. Western blotting was used to detect the expression of proteins associated with apoptosis, ferroptosis and ERS. In the hypoxia/reoxygenation (H/R) model of rat cardiomyocytes H9c2, CBX7 was highly expressed. CBX7 interference significantly protected against inflammatory response, oxidative stress, apoptosis, ferroptosis and ERS induced by H/R in H9c2 cells. Moreover, after the pretreatment with ferroptosis activator erastin or ERS agonist Tunicamycin (TM), the protective effects of CBX7 knockdown on the inflammation, oxidative stress and apoptosis in H/R-induced H9c2 cells was partially abolished. To summarize, CBX7 down-regulation may exert anti-ferroptosis and anti-ERS activities to alleviate H/R-stimulated myocardial injury. |
| doi_str_mv | 10.1007/s12013-024-01324-7 |
| format | Article |
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2+
level, respectively. Western blotting was used to detect the expression of proteins associated with apoptosis, ferroptosis and ERS. In the hypoxia/reoxygenation (H/R) model of rat cardiomyocytes H9c2, CBX7 was highly expressed. CBX7 interference significantly protected against inflammatory response, oxidative stress, apoptosis, ferroptosis and ERS induced by H/R in H9c2 cells. Moreover, after the pretreatment with ferroptosis activator erastin or ERS agonist Tunicamycin (TM), the protective effects of CBX7 knockdown on the inflammation, oxidative stress and apoptosis in H/R-induced H9c2 cells was partially abolished. To summarize, CBX7 down-regulation may exert anti-ferroptosis and anti-ERS activities to alleviate H/R-stimulated myocardial injury.</description><identifier>ISSN: 1085-9195</identifier><identifier>ISSN: 1559-0283</identifier><identifier>EISSN: 1559-0283</identifier><identifier>DOI: 10.1007/s12013-024-01324-7</identifier><identifier>PMID: 38809351</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Apoptosis ; Apoptosis - drug effects ; Assaying ; Biochemistry ; Biological and Medical Physics ; Biomedical and Life Sciences ; Biophysics ; Biotechnology ; Cardiomyocytes ; Cell Biology ; Cell Line ; Cell Survival - drug effects ; Cell viability ; Cholecystokinin ; Endoplasmic reticulum ; Endoplasmic Reticulum Stress - drug effects ; Enzyme-linked immunosorbent assay ; Ferroptosis ; Ferroptosis - drug effects ; Flow cytometry ; Hypoxia ; Inflammation ; Inflammatory response ; Injuries ; Injury analysis ; Ischemia ; Life Sciences ; Lipids ; Myocardial ischemia ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - pathology ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; Original Paper ; Oxidative stress ; Oxidative Stress - drug effects ; Pharmacology/Toxicology ; Polycomb Repressive Complex 1 - genetics ; Polycomb Repressive Complex 1 - metabolism ; Rats ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Reperfusion ; RNA Interference ; RNA, Small Interfering - metabolism ; Signal Transduction - drug effects ; Staining ; Tunicamycin ; Western blotting</subject><ispartof>Cell biochemistry and biophysics, 2024-09, Vol.82 (3), p.2171-2181</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c256t-11efb3116fc16eff4d2480eaa8da4509c801aba892adb35d808629ac01400df73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12013-024-01324-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12013-024-01324-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27929,27930,41493,42562,51324</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38809351$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Weipeng</creatorcontrib><creatorcontrib>Yan, Zeyu</creatorcontrib><creatorcontrib>Zheng, Xueou</creatorcontrib><creatorcontrib>Huang, Shiyi</creatorcontrib><creatorcontrib>Hu, Yue</creatorcontrib><creatorcontrib>Xiong, Fengjuan</creatorcontrib><creatorcontrib>He, Bufan</creatorcontrib><creatorcontrib>Wu, Yingzhi</creatorcontrib><creatorcontrib>Fu, Qiang</creatorcontrib><creatorcontrib>Li, Zhiliang</creatorcontrib><creatorcontrib>Zhou, Baihua</creatorcontrib><title>Targeting the Ferroptosis and Endoplasmic Reticulum Stress Signaling Pathways by CBX7 in Myocardial Ischemia/reperfusion Injury</title><title>Cell biochemistry and biophysics</title><addtitle>Cell Biochem Biophys</addtitle><addtitle>Cell Biochem Biophys</addtitle><description>Ferroptosis and endoplasmic reticulum stress (ERS) are common events in the process of myocardial ischemia/reperfusion injury (IRI). The suppression of chromobox7 (CBX7) has been reported to protect against ischemia/reperfusion injury, This research is purposed to expose the impacts and mechanism of CBX7 in myocardial IRI. CBX7 expression was detected using RT-qPCR and western blotting analysis. CCK-8 assay detected cell viability. Inflammatory response and oxidative stress were detected by ELISA, DCFH-DA probe and related assay kits. Flow cytometry analysis and caspase3 activity assay were used to detect cell apoptosis. C11-BODIPY 581/591 staining and ferro-orange staining were used to detect lipid reactive oxygen species (ROS) and Fe
2+
level, respectively. Western blotting was used to detect the expression of proteins associated with apoptosis, ferroptosis and ERS. In the hypoxia/reoxygenation (H/R) model of rat cardiomyocytes H9c2, CBX7 was highly expressed. CBX7 interference significantly protected against inflammatory response, oxidative stress, apoptosis, ferroptosis and ERS induced by H/R in H9c2 cells. Moreover, after the pretreatment with ferroptosis activator erastin or ERS agonist Tunicamycin (TM), the protective effects of CBX7 knockdown on the inflammation, oxidative stress and apoptosis in H/R-induced H9c2 cells was partially abolished. To summarize, CBX7 down-regulation may exert anti-ferroptosis and anti-ERS activities to alleviate H/R-stimulated myocardial injury.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Assaying</subject><subject>Biochemistry</subject><subject>Biological and Medical Physics</subject><subject>Biomedical and Life Sciences</subject><subject>Biophysics</subject><subject>Biotechnology</subject><subject>Cardiomyocytes</subject><subject>Cell Biology</subject><subject>Cell Line</subject><subject>Cell Survival - drug effects</subject><subject>Cell viability</subject><subject>Cholecystokinin</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic Reticulum Stress - drug effects</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Ferroptosis</subject><subject>Ferroptosis - drug effects</subject><subject>Flow cytometry</subject><subject>Hypoxia</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Injuries</subject><subject>Injury analysis</subject><subject>Ischemia</subject><subject>Life Sciences</subject><subject>Lipids</subject><subject>Myocardial ischemia</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Original Paper</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Pharmacology/Toxicology</subject><subject>Polycomb Repressive Complex 1 - genetics</subject><subject>Polycomb Repressive Complex 1 - metabolism</subject><subject>Rats</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Reperfusion</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Staining</subject><subject>Tunicamycin</subject><subject>Western blotting</subject><issn>1085-9195</issn><issn>1559-0283</issn><issn>1559-0283</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcFu1DAQhiMEoqXwAhyQJS5cQmdsJ3GOsGphpSIQLRK3aGI7u14lcbAToZx4dbxsAYkDF49lf_OPrS_LniO8RoDqMiIHFDlwmaea1upBdo5FUacjJR6mPagir7EuzrInMR4AOAcpH2dnQimoRYHn2Y87Cjs7u3HH5r1l1zYEP80-ushoNOxqNH7qKQ5Os88J00u_DOx2DjZGdut2I_XH1k8077_TGlm7ss3brxVzI_uwek3BOOrZNuq9HRxdBjvZ0C3R-ZFtx8MS1qfZo476aJ_d14vsy_XV3eZ9fvPx3Xbz5ibXvCjnHNF2rUAsO42l7TppuFRgiZQhWUCtFSC1pGpOphWFUaBKXpMGlACmq8RF9uqUOwX_bbFxbgYXte17Gq1fYiOgxEpJWRYJffkPevBLSD9NFCJWXACIRPETpYOPMdiumYIbKKwNQnPU05z0NElP80tPc3zFi_vopR2s-dPy20cCxAmI6Wrc2fB39n9ifwJB8JvM</recordid><startdate>20240901</startdate><enddate>20240901</enddate><creator>Jiang, Weipeng</creator><creator>Yan, Zeyu</creator><creator>Zheng, Xueou</creator><creator>Huang, Shiyi</creator><creator>Hu, Yue</creator><creator>Xiong, Fengjuan</creator><creator>He, Bufan</creator><creator>Wu, Yingzhi</creator><creator>Fu, Qiang</creator><creator>Li, Zhiliang</creator><creator>Zhou, Baihua</creator><general>Springer US</general><general>Springer Nature B.V</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>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20240901</creationdate><title>Targeting the Ferroptosis and Endoplasmic Reticulum Stress Signaling Pathways by CBX7 in Myocardial Ischemia/reperfusion Injury</title><author>Jiang, Weipeng ; Yan, Zeyu ; Zheng, Xueou ; Huang, Shiyi ; Hu, Yue ; Xiong, Fengjuan ; He, Bufan ; Wu, Yingzhi ; Fu, Qiang ; Li, Zhiliang ; Zhou, Baihua</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c256t-11efb3116fc16eff4d2480eaa8da4509c801aba892adb35d808629ac01400df73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Assaying</topic><topic>Biochemistry</topic><topic>Biological and Medical Physics</topic><topic>Biomedical and Life Sciences</topic><topic>Biophysics</topic><topic>Biotechnology</topic><topic>Cardiomyocytes</topic><topic>Cell Biology</topic><topic>Cell Line</topic><topic>Cell Survival - drug effects</topic><topic>Cell viability</topic><topic>Cholecystokinin</topic><topic>Endoplasmic reticulum</topic><topic>Endoplasmic Reticulum Stress - drug effects</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Ferroptosis</topic><topic>Ferroptosis - drug effects</topic><topic>Flow cytometry</topic><topic>Hypoxia</topic><topic>Inflammation</topic><topic>Inflammatory response</topic><topic>Injuries</topic><topic>Injury analysis</topic><topic>Ischemia</topic><topic>Life Sciences</topic><topic>Lipids</topic><topic>Myocardial ischemia</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - pathology</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Original Paper</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Pharmacology/Toxicology</topic><topic>Polycomb Repressive Complex 1 - genetics</topic><topic>Polycomb Repressive Complex 1 - metabolism</topic><topic>Rats</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Reperfusion</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Staining</topic><topic>Tunicamycin</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Weipeng</creatorcontrib><creatorcontrib>Yan, Zeyu</creatorcontrib><creatorcontrib>Zheng, Xueou</creatorcontrib><creatorcontrib>Huang, Shiyi</creatorcontrib><creatorcontrib>Hu, Yue</creatorcontrib><creatorcontrib>Xiong, Fengjuan</creatorcontrib><creatorcontrib>He, Bufan</creatorcontrib><creatorcontrib>Wu, Yingzhi</creatorcontrib><creatorcontrib>Fu, Qiang</creatorcontrib><creatorcontrib>Li, Zhiliang</creatorcontrib><creatorcontrib>Zhou, Baihua</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell biochemistry and biophysics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Weipeng</au><au>Yan, Zeyu</au><au>Zheng, Xueou</au><au>Huang, Shiyi</au><au>Hu, Yue</au><au>Xiong, Fengjuan</au><au>He, Bufan</au><au>Wu, Yingzhi</au><au>Fu, Qiang</au><au>Li, Zhiliang</au><au>Zhou, Baihua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Targeting the Ferroptosis and Endoplasmic Reticulum Stress Signaling Pathways by CBX7 in Myocardial Ischemia/reperfusion Injury</atitle><jtitle>Cell biochemistry and biophysics</jtitle><stitle>Cell Biochem Biophys</stitle><addtitle>Cell Biochem Biophys</addtitle><date>2024-09-01</date><risdate>2024</risdate><volume>82</volume><issue>3</issue><spage>2171</spage><epage>2181</epage><pages>2171-2181</pages><issn>1085-9195</issn><issn>1559-0283</issn><eissn>1559-0283</eissn><abstract>Ferroptosis and endoplasmic reticulum stress (ERS) are common events in the process of myocardial ischemia/reperfusion injury (IRI). The suppression of chromobox7 (CBX7) has been reported to protect against ischemia/reperfusion injury, This research is purposed to expose the impacts and mechanism of CBX7 in myocardial IRI. CBX7 expression was detected using RT-qPCR and western blotting analysis. CCK-8 assay detected cell viability. Inflammatory response and oxidative stress were detected by ELISA, DCFH-DA probe and related assay kits. Flow cytometry analysis and caspase3 activity assay were used to detect cell apoptosis. C11-BODIPY 581/591 staining and ferro-orange staining were used to detect lipid reactive oxygen species (ROS) and Fe
2+
level, respectively. Western blotting was used to detect the expression of proteins associated with apoptosis, ferroptosis and ERS. In the hypoxia/reoxygenation (H/R) model of rat cardiomyocytes H9c2, CBX7 was highly expressed. CBX7 interference significantly protected against inflammatory response, oxidative stress, apoptosis, ferroptosis and ERS induced by H/R in H9c2 cells. Moreover, after the pretreatment with ferroptosis activator erastin or ERS agonist Tunicamycin (TM), the protective effects of CBX7 knockdown on the inflammation, oxidative stress and apoptosis in H/R-induced H9c2 cells was partially abolished. To summarize, CBX7 down-regulation may exert anti-ferroptosis and anti-ERS activities to alleviate H/R-stimulated myocardial injury.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>38809351</pmid><doi>10.1007/s12013-024-01324-7</doi><tpages>11</tpages></addata></record> |
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| subjects | Animals Apoptosis Apoptosis - drug effects Assaying Biochemistry Biological and Medical Physics Biomedical and Life Sciences Biophysics Biotechnology Cardiomyocytes Cell Biology Cell Line Cell Survival - drug effects Cell viability Cholecystokinin Endoplasmic reticulum Endoplasmic Reticulum Stress - drug effects Enzyme-linked immunosorbent assay Ferroptosis Ferroptosis - drug effects Flow cytometry Hypoxia Inflammation Inflammatory response Injuries Injury analysis Ischemia Life Sciences Lipids Myocardial ischemia Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Original Paper Oxidative stress Oxidative Stress - drug effects Pharmacology/Toxicology Polycomb Repressive Complex 1 - genetics Polycomb Repressive Complex 1 - metabolism Rats Reactive oxygen species Reactive Oxygen Species - metabolism Reperfusion RNA Interference RNA, Small Interfering - metabolism Signal Transduction - drug effects Staining Tunicamycin Western blotting |
| title | Targeting the Ferroptosis and Endoplasmic Reticulum Stress Signaling Pathways by CBX7 in Myocardial Ischemia/reperfusion Injury |
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