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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from DOX(doxorubicin) -treated wild type or CHIP knockout C57BL/6J mice at day 5

ABSTRACT: The clinical application of doxorubicin as a broad-spectrum anti-tumor antibiotic is limited greatly by its cardiotoxicity. Various mechanisms have been studied, but little is known about whether genes or pathways relevant with energy metabolism contributes to doxorubicin-induced cardiomyopathy or not. We used microarrays to detail the global expression profiling of acute cardiomyopathy induced by doxorubicin in wild type or CHIP knockout C57BL/6J mice and discovered distinct classes of changed genes during this process. The whole hearts were selected for RNA extraction and hybridization on Affymetrix microarrays at day 5 after a single intraperitoneal injection of doxorubicin at a dose of 15 mg/kg.

ORGANISM(S): Mus musculus

SUBMITTER: zhang long

PROVIDER: E-GEOD-59672 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from DOX(doxorubicin) -treated wild type or CHIP knockout C57BL/6J mice at day 5

Project description:The clinical application of doxorubicin as a broad-spectrum anti-tumor antibiotic is limited greatly by its cardiotoxicity. Various mechanisms have been studied, but little is known about whether genes or pathways relevant with energy metabolism contributes to doxorubicin-induced cardiomyopathy or not. We used microarrays to detail the global expression profiling of acute cardiomyopathy induced by doxorubicin in wild type or CHIP knockout C57BL/6J mice and discovered distinct classes of changed genes during this process.

2014-07-23 | GSE59672 | GEO

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2014-08-08 | PXD001211 | Pride

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The Cardiac Endothelial Cell cGAS-STING Pathway Promotes Doxorubicin-Induced Cardiotoxicity via CD38-Mediated NAD Decline and Mitochondrial Dysfunction [mouse]

2023-03-02 | GSE226114 | GEO

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Project description:Improvements in the diagnosis and treatment of cancer has revealed the long-term side effects of chemotherapeutics, particularly cardiotoxicity. Current clinical measures to track cardiotoxicity are insufficient to diagnose damage before it has been done, necessitating new, early biomarkers of cardiotoxicity. Here, we collected paired transcriptomics and metabolomics data characterizing in vitro cardiotoxicity to three compounds: 5-fluorouracil, acetaminophen, and doxorubicin. Standard gene enrichment and metabolomics approaches identify some commonly affected pathways and metabolites but are not able to readily identify mechanisms of cardiotoxicity. Here, we integrate this paired data with a genome-scale metabolic network reconstruction (GENRE) of the heart to identify shifted metabolic functions, unique metabolic reactions, and changes in flux in metabolic reactions in response to these compounds. Using this approach, we are able to confirm known mechanisms of doxorubicin-induced cardiotoxicity and provide hypotheses for mechanisms of cardiotoxicity for 5-fluorouracil and acetaminophen.

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