{"title":"p53在阿霉素诱导的心肌病作为线粒体疾病中的保护作用。","authors":"Masahiro Nishi, Ping-Yuan Wang, Paul M Hwang","doi":"10.1080/23723556.2020.1724598","DOIUrl":null,"url":null,"abstract":"<p><p>Doxorubicin is widely used against cancer but carries the risk of a progressive cardiomyopathy associated with mitochondrial loss. Using genetic models, our recent study demonstrates that mitochondrial genomic DNA regulation by tumor protein p53 (TP53, best known as p53) prevents the cardiotoxicity of low dose doxorubicin which does not activate the p53-dependent cell death pathway.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1724598"},"PeriodicalIF":0.0000,"publicationDate":"2020-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1724598","citationCount":"2","resultStr":"{\"title\":\"Protective role of p53 in doxorubicin-induced cardiomyopathy as a mitochondrial disease.\",\"authors\":\"Masahiro Nishi, Ping-Yuan Wang, Paul M Hwang\",\"doi\":\"10.1080/23723556.2020.1724598\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Doxorubicin is widely used against cancer but carries the risk of a progressive cardiomyopathy associated with mitochondrial loss. Using genetic models, our recent study demonstrates that mitochondrial genomic DNA regulation by tumor protein p53 (TP53, best known as p53) prevents the cardiotoxicity of low dose doxorubicin which does not activate the p53-dependent cell death pathway.</p>\",\"PeriodicalId\":520710,\"journal\":{\"name\":\"Molecular & cellular oncology\",\"volume\":\" \",\"pages\":\"1724598\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-02-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1080/23723556.2020.1724598\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular & cellular oncology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1080/23723556.2020.1724598\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2020/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular & cellular oncology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/23723556.2020.1724598","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2020/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
Protective role of p53 in doxorubicin-induced cardiomyopathy as a mitochondrial disease.
Doxorubicin is widely used against cancer but carries the risk of a progressive cardiomyopathy associated with mitochondrial loss. Using genetic models, our recent study demonstrates that mitochondrial genomic DNA regulation by tumor protein p53 (TP53, best known as p53) prevents the cardiotoxicity of low dose doxorubicin which does not activate the p53-dependent cell death pathway.
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