Comprehensive analysis of transcriptomics and metabolomics to understand chronic ethanol induced murine cardiotoxicity

Alcohol abuse has attracted public attention and long-term alcohol exposure can lead to alcohol-featured non-ischemic dilated cardiomyopathy. However, the precise underlying mechanisms of alcoholic cardiomyopathy remain to be elucidated. This study aimed to comprehensively characterize alcohol abuse...

Full description

Saved in:
Bibliographic Details
Published in:Molecular and cellular biochemistry 2023-06, Vol.478 (6), p.1345-1359
Main Authors: Xue, Qiupeng, Liu, Xiaochen, Zhu, Rongzhe, Zhang, Tianyi, Dong, Xiaoru, Jiang, Yan
Format: Article
Language:English
Subjects:
Abuse
Acetaldehyde
Actin
Alcohol
Alcohol abuse
Alcohol, Denatured
Alcoholism
Alcohols
Amino acids
Animals
Annotations
Antigen presentation
Antigen processing
Antigens
Biochemistry
Biomarkers
Biomedical and Life Sciences
Cancer Research
Cardiology
Cardiomyocytes
Cardiomyopathy
Cardiotoxicity
Cytoskeleton
Dilated cardiomyopathy
Drug abuse
Energy metabolism
Ethanol
Ethanol - toxicity
Fibrosis
Genes
Genetic transcription
Hypertrophy
Injury analysis
Intoxication
Ischemia
Life Sciences
Lipid metabolism
Lipids
Male
Medical Biochemistry
Metabolism
Metabolites
Metabolomics
Mice
Mice, Inbred C57BL
MicroRNA
MicroRNAs
miRNA
Nucleotides
Oxidative stress
Ribonucleic acid
RNA
Signal transduction
Signaling
Transcriptome
Transcriptomics
Tyrosine
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c442t-d0b4b11b087d5903a840fdca722ec57d9012de3af4c80fcb3755d78c6145e8173
cites cdi_FETCH-LOGICAL-c442t-d0b4b11b087d5903a840fdca722ec57d9012de3af4c80fcb3755d78c6145e8173
container_end_page 1359
container_issue 6
container_start_page 1345
container_title Molecular and cellular biochemistry
container_volume 478
creator Xue, Qiupeng
Liu, Xiaochen
Zhu, Rongzhe
Zhang, Tianyi
Dong, Xiaoru
Jiang, Yan
description Alcohol abuse has attracted public attention and long-term alcohol exposure can lead to alcohol-featured non-ischemic dilated cardiomyopathy. However, the precise underlying mechanisms of alcoholic cardiomyopathy remain to be elucidated. This study aimed to comprehensively characterize alcohol abuse-mediated effects on downstream metabolites and genes transcription using a multi-omics strategy. We established chronic ethanol intoxication model in adult male C57BL/6 mice through 8 weeks of 95% alcohol vapor administration and performed metabolomics analysis, mRNA-seq and microRNA-seq analysis with myocardial tissues. Firstly, ethanol markedly induced ejection fraction reductions, cardiomyocyte hypertrophy, and myocardial fibrosis in mice with myocardial oxidative injury. In addition, the omics analysis identified a total of 166 differentially expressed metabolites (DEMs), 241 differentially expressed genes (DEGs) and 19 differentially expressed microRNAs (DEmiRNAs), respectively. The results highlighted that alcohol abuse mainly interfered with endogenous lipids, amino acids and nucleotides production and the relevant genes transcription in mice hearts. Based on KEGG database, the affected signaling pathways are primarily mapped to the antigen processing and presentation, regulation of actin cytoskeleton, AMPK signaling pathway, tyrosine metabolism and PPAR signaling pathway, etc. Furthermore, 9 hub genes related to oxidative stress from DEGs were selected based on function annotation, and potential alcoholic cardiotoxic oxidative stress biomarkers were determined through establishing PPI network and DEmiRNAs-DEGs cross-talk. Altogether, our data strongly supported the conclusion that ethanol abuse characteristically affected amino acid and energy metabolism, nucleotide metabolism and especially lipids metabolism in mice hearts, and underlined the values of lipids signaling and oxidative stress in the treatment strategies.
doi_str_mv 10.1007/s11010-022-04592-0
format article
fullrecord <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_journals_2810251902</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A748397956</galeid><sourcerecordid>A748397956</sourcerecordid><originalsourceid>FETCH-LOGICAL-c442t-d0b4b11b087d5903a840fdca722ec57d9012de3af4c80fcb3755d78c6145e8173</originalsourceid><addsrcrecordid>eNp9kV9rFTEQxYNY7G31C_ggCz5vnfy72X0sF62Fgi_2OWST2d6U3eSaZIv325t2q0UQCSQw8zvDnBxC3lO4oADqU6YUKLTAWAtC9vV-RTZUKt6KnvavyQY4QNtRpU7JWc73UGmg9A055VsOfdfxDXnYxfmQcI8h-wdsTDDTMfvcxLEpyYRskz-UOHuba881MxYzxGktlNgswWHK5bFl9ykGbxssexPi1PjgFotVsiQfsLEmOR9L_OmtL8e35GQ0U8Z3z-85uf3y-fvua3vz7ep6d3nTWiFYaR0MYqB0gE452QM3nYDRWaMYQyuV64Eyh9yMwnYw2oErKZ3q7JYKidU4Pycf17mHFH8smIu-j0uqJrNmHQUmaQ_shbozE2ofxli929lnqy-V6Hivermt1MU_qHoc1u-IAUdf638J2CqwKeaccNSH5GeTjpqCfkxQrwnqmqB-SlBDFX143ngZZnR_JL8jqwBfgVxb4Q7Ti6X_jP0FFnqnlw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2810251902</pqid></control><display><type>article</type><title>Comprehensive analysis of transcriptomics and metabolomics to understand chronic ethanol induced murine cardiotoxicity</title><source>Springer Nature</source><creator>Xue, Qiupeng ; Liu, Xiaochen ; Zhu, Rongzhe ; Zhang, Tianyi ; Dong, Xiaoru ; Jiang, Yan</creator><creatorcontrib>Xue, Qiupeng ; Liu, Xiaochen ; Zhu, Rongzhe ; Zhang, Tianyi ; Dong, Xiaoru ; Jiang, Yan</creatorcontrib><description>Alcohol abuse has attracted public attention and long-term alcohol exposure can lead to alcohol-featured non-ischemic dilated cardiomyopathy. However, the precise underlying mechanisms of alcoholic cardiomyopathy remain to be elucidated. This study aimed to comprehensively characterize alcohol abuse-mediated effects on downstream metabolites and genes transcription using a multi-omics strategy. We established chronic ethanol intoxication model in adult male C57BL/6 mice through 8 weeks of 95% alcohol vapor administration and performed metabolomics analysis, mRNA-seq and microRNA-seq analysis with myocardial tissues. Firstly, ethanol markedly induced ejection fraction reductions, cardiomyocyte hypertrophy, and myocardial fibrosis in mice with myocardial oxidative injury. In addition, the omics analysis identified a total of 166 differentially expressed metabolites (DEMs), 241 differentially expressed genes (DEGs) and 19 differentially expressed microRNAs (DEmiRNAs), respectively. The results highlighted that alcohol abuse mainly interfered with endogenous lipids, amino acids and nucleotides production and the relevant genes transcription in mice hearts. Based on KEGG database, the affected signaling pathways are primarily mapped to the antigen processing and presentation, regulation of actin cytoskeleton, AMPK signaling pathway, tyrosine metabolism and PPAR signaling pathway, etc. Furthermore, 9 hub genes related to oxidative stress from DEGs were selected based on function annotation, and potential alcoholic cardiotoxic oxidative stress biomarkers were determined through establishing PPI network and DEmiRNAs-DEGs cross-talk. Altogether, our data strongly supported the conclusion that ethanol abuse characteristically affected amino acid and energy metabolism, nucleotide metabolism and especially lipids metabolism in mice hearts, and underlined the values of lipids signaling and oxidative stress in the treatment strategies.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-022-04592-0</identifier><identifier>PMID: 36309883</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Abuse ; Acetaldehyde ; Actin ; Alcohol ; Alcohol abuse ; Alcohol, Denatured ; Alcoholism ; Alcohols ; Amino acids ; Animals ; Annotations ; Antigen presentation ; Antigen processing ; Antigens ; Biochemistry ; Biomarkers ; Biomedical and Life Sciences ; Cancer Research ; Cardiology ; Cardiomyocytes ; Cardiomyopathy ; Cardiotoxicity ; Cytoskeleton ; Dilated cardiomyopathy ; Drug abuse ; Energy metabolism ; Ethanol ; Ethanol - toxicity ; Fibrosis ; Genes ; Genetic transcription ; Hypertrophy ; Injury analysis ; Intoxication ; Ischemia ; Life Sciences ; Lipid metabolism ; Lipids ; Male ; Medical Biochemistry ; Metabolism ; Metabolites ; Metabolomics ; Mice ; Mice, Inbred C57BL ; MicroRNA ; MicroRNAs ; miRNA ; Nucleotides ; Oxidative stress ; Ribonucleic acid ; RNA ; Signal transduction ; Signaling ; Transcriptome ; Transcriptomics ; Tyrosine</subject><ispartof>Molecular and cellular biochemistry, 2023-06, Vol.478 (6), p.1345-1359</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022. 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>2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>COPYRIGHT 2023 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-d0b4b11b087d5903a840fdca722ec57d9012de3af4c80fcb3755d78c6145e8173</citedby><cites>FETCH-LOGICAL-c442t-d0b4b11b087d5903a840fdca722ec57d9012de3af4c80fcb3755d78c6145e8173</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27900,27901</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36309883$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xue, Qiupeng</creatorcontrib><creatorcontrib>Liu, Xiaochen</creatorcontrib><creatorcontrib>Zhu, Rongzhe</creatorcontrib><creatorcontrib>Zhang, Tianyi</creatorcontrib><creatorcontrib>Dong, Xiaoru</creatorcontrib><creatorcontrib>Jiang, Yan</creatorcontrib><title>Comprehensive analysis of transcriptomics and metabolomics to understand chronic ethanol induced murine cardiotoxicity</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>Alcohol abuse has attracted public attention and long-term alcohol exposure can lead to alcohol-featured non-ischemic dilated cardiomyopathy. However, the precise underlying mechanisms of alcoholic cardiomyopathy remain to be elucidated. This study aimed to comprehensively characterize alcohol abuse-mediated effects on downstream metabolites and genes transcription using a multi-omics strategy. We established chronic ethanol intoxication model in adult male C57BL/6 mice through 8 weeks of 95% alcohol vapor administration and performed metabolomics analysis, mRNA-seq and microRNA-seq analysis with myocardial tissues. Firstly, ethanol markedly induced ejection fraction reductions, cardiomyocyte hypertrophy, and myocardial fibrosis in mice with myocardial oxidative injury. In addition, the omics analysis identified a total of 166 differentially expressed metabolites (DEMs), 241 differentially expressed genes (DEGs) and 19 differentially expressed microRNAs (DEmiRNAs), respectively. The results highlighted that alcohol abuse mainly interfered with endogenous lipids, amino acids and nucleotides production and the relevant genes transcription in mice hearts. Based on KEGG database, the affected signaling pathways are primarily mapped to the antigen processing and presentation, regulation of actin cytoskeleton, AMPK signaling pathway, tyrosine metabolism and PPAR signaling pathway, etc. Furthermore, 9 hub genes related to oxidative stress from DEGs were selected based on function annotation, and potential alcoholic cardiotoxic oxidative stress biomarkers were determined through establishing PPI network and DEmiRNAs-DEGs cross-talk. Altogether, our data strongly supported the conclusion that ethanol abuse characteristically affected amino acid and energy metabolism, nucleotide metabolism and especially lipids metabolism in mice hearts, and underlined the values of lipids signaling and oxidative stress in the treatment strategies.</description><subject>Abuse</subject><subject>Acetaldehyde</subject><subject>Actin</subject><subject>Alcohol</subject><subject>Alcohol abuse</subject><subject>Alcohol, Denatured</subject><subject>Alcoholism</subject><subject>Alcohols</subject><subject>Amino acids</subject><subject>Animals</subject><subject>Annotations</subject><subject>Antigen presentation</subject><subject>Antigen processing</subject><subject>Antigens</subject><subject>Biochemistry</subject><subject>Biomarkers</subject><subject>Biomedical and Life Sciences</subject><subject>Cancer Research</subject><subject>Cardiology</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathy</subject><subject>Cardiotoxicity</subject><subject>Cytoskeleton</subject><subject>Dilated cardiomyopathy</subject><subject>Drug abuse</subject><subject>Energy metabolism</subject><subject>Ethanol</subject><subject>Ethanol - toxicity</subject><subject>Fibrosis</subject><subject>Genes</subject><subject>Genetic transcription</subject><subject>Hypertrophy</subject><subject>Injury analysis</subject><subject>Intoxication</subject><subject>Ischemia</subject><subject>Life Sciences</subject><subject>Lipid metabolism</subject><subject>Lipids</subject><subject>Male</subject><subject>Medical Biochemistry</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Metabolomics</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>miRNA</subject><subject>Nucleotides</subject><subject>Oxidative stress</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Transcriptome</subject><subject>Transcriptomics</subject><subject>Tyrosine</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNp9kV9rFTEQxYNY7G31C_ggCz5vnfy72X0sF62Fgi_2OWST2d6U3eSaZIv325t2q0UQCSQw8zvDnBxC3lO4oADqU6YUKLTAWAtC9vV-RTZUKt6KnvavyQY4QNtRpU7JWc73UGmg9A055VsOfdfxDXnYxfmQcI8h-wdsTDDTMfvcxLEpyYRskz-UOHuba881MxYzxGktlNgswWHK5bFl9ykGbxssexPi1PjgFotVsiQfsLEmOR9L_OmtL8e35GQ0U8Z3z-85uf3y-fvua3vz7ep6d3nTWiFYaR0MYqB0gE452QM3nYDRWaMYQyuV64Eyh9yMwnYw2oErKZ3q7JYKidU4Pycf17mHFH8smIu-j0uqJrNmHQUmaQ_shbozE2ofxli929lnqy-V6Hivermt1MU_qHoc1u-IAUdf638J2CqwKeaccNSH5GeTjpqCfkxQrwnqmqB-SlBDFX143ngZZnR_JL8jqwBfgVxb4Q7Ti6X_jP0FFnqnlw</recordid><startdate>20230601</startdate><enddate>20230601</enddate><creator>Xue, Qiupeng</creator><creator>Liu, Xiaochen</creator><creator>Zhu, Rongzhe</creator><creator>Zhang, Tianyi</creator><creator>Dong, Xiaoru</creator><creator>Jiang, Yan</creator><general>Springer US</general><general>Springer</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>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>20230601</creationdate><title>Comprehensive analysis of transcriptomics and metabolomics to understand chronic ethanol induced murine cardiotoxicity</title><author>Xue, Qiupeng ; Liu, Xiaochen ; Zhu, Rongzhe ; Zhang, Tianyi ; Dong, Xiaoru ; Jiang, Yan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-d0b4b11b087d5903a840fdca722ec57d9012de3af4c80fcb3755d78c6145e8173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Abuse</topic><topic>Acetaldehyde</topic><topic>Actin</topic><topic>Alcohol</topic><topic>Alcohol abuse</topic><topic>Alcohol, Denatured</topic><topic>Alcoholism</topic><topic>Alcohols</topic><topic>Amino acids</topic><topic>Animals</topic><topic>Annotations</topic><topic>Antigen presentation</topic><topic>Antigen processing</topic><topic>Antigens</topic><topic>Biochemistry</topic><topic>Biomarkers</topic><topic>Biomedical and Life Sciences</topic><topic>Cancer Research</topic><topic>Cardiology</topic><topic>Cardiomyocytes</topic><topic>Cardiomyopathy</topic><topic>Cardiotoxicity</topic><topic>Cytoskeleton</topic><topic>Dilated cardiomyopathy</topic><topic>Drug abuse</topic><topic>Energy metabolism</topic><topic>Ethanol</topic><topic>Ethanol - toxicity</topic><topic>Fibrosis</topic><topic>Genes</topic><topic>Genetic transcription</topic><topic>Hypertrophy</topic><topic>Injury analysis</topic><topic>Intoxication</topic><topic>Ischemia</topic><topic>Life Sciences</topic><topic>Lipid metabolism</topic><topic>Lipids</topic><topic>Male</topic><topic>Medical Biochemistry</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Metabolomics</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>miRNA</topic><topic>Nucleotides</topic><topic>Oxidative stress</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Transcriptome</topic><topic>Transcriptomics</topic><topic>Tyrosine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xue, Qiupeng</creatorcontrib><creatorcontrib>Liu, Xiaochen</creatorcontrib><creatorcontrib>Zhu, Rongzhe</creatorcontrib><creatorcontrib>Zhang, Tianyi</creatorcontrib><creatorcontrib>Dong, Xiaoru</creatorcontrib><creatorcontrib>Jiang, Yan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health Medical collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Science Journals</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health &amp; Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health &amp; Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied &amp; Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xue, Qiupeng</au><au>Liu, Xiaochen</au><au>Zhu, Rongzhe</au><au>Zhang, Tianyi</au><au>Dong, Xiaoru</au><au>Jiang, Yan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Comprehensive analysis of transcriptomics and metabolomics to understand chronic ethanol induced murine cardiotoxicity</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2023-06-01</date><risdate>2023</risdate><volume>478</volume><issue>6</issue><spage>1345</spage><epage>1359</epage><pages>1345-1359</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>Alcohol abuse has attracted public attention and long-term alcohol exposure can lead to alcohol-featured non-ischemic dilated cardiomyopathy. However, the precise underlying mechanisms of alcoholic cardiomyopathy remain to be elucidated. This study aimed to comprehensively characterize alcohol abuse-mediated effects on downstream metabolites and genes transcription using a multi-omics strategy. We established chronic ethanol intoxication model in adult male C57BL/6 mice through 8 weeks of 95% alcohol vapor administration and performed metabolomics analysis, mRNA-seq and microRNA-seq analysis with myocardial tissues. Firstly, ethanol markedly induced ejection fraction reductions, cardiomyocyte hypertrophy, and myocardial fibrosis in mice with myocardial oxidative injury. In addition, the omics analysis identified a total of 166 differentially expressed metabolites (DEMs), 241 differentially expressed genes (DEGs) and 19 differentially expressed microRNAs (DEmiRNAs), respectively. The results highlighted that alcohol abuse mainly interfered with endogenous lipids, amino acids and nucleotides production and the relevant genes transcription in mice hearts. Based on KEGG database, the affected signaling pathways are primarily mapped to the antigen processing and presentation, regulation of actin cytoskeleton, AMPK signaling pathway, tyrosine metabolism and PPAR signaling pathway, etc. Furthermore, 9 hub genes related to oxidative stress from DEGs were selected based on function annotation, and potential alcoholic cardiotoxic oxidative stress biomarkers were determined through establishing PPI network and DEmiRNAs-DEGs cross-talk. Altogether, our data strongly supported the conclusion that ethanol abuse characteristically affected amino acid and energy metabolism, nucleotide metabolism and especially lipids metabolism in mice hearts, and underlined the values of lipids signaling and oxidative stress in the treatment strategies.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>36309883</pmid><doi>10.1007/s11010-022-04592-0</doi><tpages>15</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0300-8177
ispartof Molecular and cellular biochemistry, 2023-06, Vol.478 (6), p.1345-1359
issn 0300-8177
1573-4919
language eng
recordid cdi_proquest_journals_2810251902
source Springer Nature
subjects Abuse
Acetaldehyde
Actin
Alcohol
Alcohol abuse
Alcohol, Denatured
Alcoholism
Alcohols
Amino acids
Animals
Annotations
Antigen presentation
Antigen processing
Antigens
Biochemistry
Biomarkers
Biomedical and Life Sciences
Cancer Research
Cardiology
Cardiomyocytes
Cardiomyopathy
Cardiotoxicity
Cytoskeleton
Dilated cardiomyopathy
Drug abuse
Energy metabolism
Ethanol
Ethanol - toxicity
Fibrosis
Genes
Genetic transcription
Hypertrophy
Injury analysis
Intoxication
Ischemia
Life Sciences
Lipid metabolism
Lipids
Male
Medical Biochemistry
Metabolism
Metabolites
Metabolomics
Mice
Mice, Inbred C57BL
MicroRNA
MicroRNAs
miRNA
Nucleotides
Oxidative stress
Ribonucleic acid
RNA
Signal transduction
Signaling
Transcriptome
Transcriptomics
Tyrosine
title Comprehensive analysis of transcriptomics and metabolomics to understand chronic ethanol induced murine cardiotoxicity
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-24T21%3A06%3A07IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Comprehensive%20analysis%20of%20transcriptomics%20and%20metabolomics%20to%20understand%20chronic%20ethanol%20induced%20murine%20cardiotoxicity&rft.jtitle=Molecular%20and%20cellular%20biochemistry&rft.au=Xue,%20Qiupeng&rft.date=2023-06-01&rft.volume=478&rft.issue=6&rft.spage=1345&rft.epage=1359&rft.pages=1345-1359&rft.issn=0300-8177&rft.eissn=1573-4919&rft_id=info:doi/10.1007/s11010-022-04592-0&rft_dat=%3Cgale_proqu%3EA748397956%3C/gale_proqu%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c442t-d0b4b11b087d5903a840fdca722ec57d9012de3af4c80fcb3755d78c6145e8173%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2810251902&rft_id=info:pmid/36309883&rft_galeid=A748397956&rfr_iscdi=true