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慢性酒精暴露导致的心肌损伤——一项基于蛋白质组学的初步研究。

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

机构信息

Department of Forensic Pathology, School of Forensic Medicine, China Medical University, Shenyang 110122, China.

The Third Clinical Department, China Medical University, Shenyang 110122, China.

出版信息

Molecules. 2022 Jul 3;27(13):4284. doi: 10.3390/molecules27134284.

DOI:10.3390/molecules27134284
PMID:35807529
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9268295/
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.

摘要

慢性酒精暴露可导致心肌退行性疾病,表现为心脏功能不全、心律失常等,这些被定义为酒精性心肌病(ACM)。先前已经通过代谢组学研究了酒精介导的心肌损伤,并且已经证明其涉及与不饱和脂肪酸生物合成和氧化磷酸化有关的京都基因与基因组百科全书(KEGG)途径,这初步探讨了慢性饮酒引起的 ACM 的机制。为了进一步研究酒精引起的心肌损伤,对先前成功建立的 ACM 小鼠模型的心肌标本进行了组织学、超声心动图和蛋白质组学分析,并通过实时定量聚合酶链反应(qPCR)进行了验证。组织病理学和超声心动图结果显示心肌细胞肥大、心室扩张和心功能下降。通过 ProteomeXchange 可获得的蛋白质组学结果,鉴定到 56 个差异表达蛋白(DEPs),这些蛋白可能参与与脂肪酸生物合成紊乱、脂质代谢紊乱、氧化应激相关的 KEGG 途径,最终导致扩张型心肌病(DCM)的发生。本研究进一步阐明了慢性酒精摄入导致心肌损伤的潜在影响,为进一步阐明 ACM 的潜在机制奠定了基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ebb/9268295/fa9598495b37/molecules-27-04284-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ebb/9268295/1ac102cc9303/molecules-27-04284-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ebb/9268295/0066e684d068/molecules-27-04284-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ebb/9268295/9edefc54ef4f/molecules-27-04284-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ebb/9268295/64bf8af156d5/molecules-27-04284-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ebb/9268295/fa9598495b37/molecules-27-04284-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ebb/9268295/1ac102cc9303/molecules-27-04284-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ebb/9268295/0066e684d068/molecules-27-04284-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ebb/9268295/036de5c398d3/molecules-27-04284-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ebb/9268295/9edefc54ef4f/molecules-27-04284-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ebb/9268295/64bf8af156d5/molecules-27-04284-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ebb/9268295/fa9598495b37/molecules-27-04284-g006.jpg

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