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pmid:35807529

Myocardial Injury Caused by Chronic Alcohol Exposure-A Pilot Study Based on Proteomics.

Xiaonan Ma · Zihan Liao · Rongxuan Li · Wei Xia · Honghui Guo · Jiawei Luo · Huaxin Sheng · Meihui Tian · Zhipeng Cao

Molecules (Basel, Switzerland) · 2022 doi:10.3390/molecules27134284

Paper

complete

Experiment

complete

Data

partial

Analysis

complete

Execution

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title
Myocardial Injury Caused by Chronic Alcohol Exposure-A Pilot Study Based on Proteomics.
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10.3390/molecules27134284
pmid
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Xiaonan Ma
[1]
Zihan Liao
[2]
Rongxuan Li
[3]
Wei Xia
[4]
Honghui Guo
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Jiawei Luo
[6]
Huaxin Sheng
[7]
Meihui Tian
[8]
Zhipeng Cao
journal
Molecules (Basel, Switzerland)
year
2022
abstract
Chronic alcohol exposure can cause myocardial degenerative diseases, manifested as cardiac insufficiency, arrhythmia, etc. These are defined as alcoholic cardiomyopathy (ACM). Alcohol-mediated myocardial injury has previously been studied through metabolomics, and it has been proved to be involved in the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway concerning unsaturated fatty acids biosynthesis and oxidative phosphorylation, which tentatively explored the mechanism of ACM induced by chronic drinking. To further study alcohol-induced myocardial injury, myocardial specimens from a previously successfully established mouse model of ACM were subjected to histological, echocardiographic, and proteomic analyses, and validated by real-time quantitative polymerase chain reaction (qPCR). Results of histopathology and echocardiography showed the hypertrophy of cardiomyocytes, the dilation of ventricles, and decreased cardiac function. Proteomic results, available via ProteomeXchange with identifier PXD032949, revealed 56 differentially expressed proteins (DEPs) were identified, which have the potential to be involved in the KEGG pathway related to fatty acid biosynthesis disorders, lipid metabolism disorders, oxidative stress, and, ultimately, in the development of dilated cardiomyopathy (DCM). The present study further elucidates the underlying effects of myocardial injury due to chronic alcohol intake, laying a foundation for further studies to clarify the potential mechanisms of ACM.
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PCA analysis showed a good separation between the ACM group and the control group (Figure 2). PC1 and PC2 represented 47.79% and 22.26%, respectively, of the total variability in the data set.
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PCA analysis showed a good separation between the ACM group and the control group (Figure 2). PC1 and PC2 represented 47.79% and 22.26%, respectively, of the total variability in the data set.
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