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急性心肌梗死中与细胞衰老和线粒体相关的关键基因的鉴定

Identification of key genes associated with cellular aging and mitochondria in acute myocardial infarction.

作者信息

Chen Dehong, Yao Lingling, Mo Ke, Li Linan, Liu Zhiheng, Xia Zhengyuan, Ding Hanlin

机构信息

Department of Urology, Shenzhen Guangming District People's Hospital, Shenzhen, 518106, Guangdong, China.

Department of Anesthesiology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, 441021, China.

出版信息

Sci Rep. 2025 Jul 1;15(1):21384. doi: 10.1038/s41598-025-05849-6.


DOI:10.1038/s41598-025-05849-6
PMID:40594763
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12216652/
Abstract

Acute myocardial infarction (AMI) poses a significant global mortality burden. Utilizing bio informatics, this study explored cellular aging-related genes (CARGs) and mitochondrial-related genes (MRGs). in AMI Public AMI datasets were analyzed using differential expression and weighted gene co-expression network analysis (WGCNA) to identify 1,373 differentially expressed genes (DEGs), of which 643 were upregulated and 730 downregulated. A turquoise module related to cellular aging was identified by gene set variation analysis (WGCNA). Venn analysis revealed 37 candidate genes intersecting DEGs, key module genes, and MRGs. Machine learning, receiver operating characteristic (ROC) analysis, and reverse transcription quantitative polymerase chain reaction (RT-qPCR) validated Isopentenyl-diphosphate delta-isomerase 1 (IDI1) and phorbol-12-myristate-13-acetate-induced protein 1 (PMAIP1) as key AMI genes. A comprehensive lncRNA-miRNA-mRNA network was constructed, and Cyclosporine showed strong binding affinities with IDI1 (-6.2 kcal/mol) and PMAIP1 (-4.8 kcal/mol), indicating therapeutic potential. This study may provide insights into AMI pathogenesis and highlight potential drug targets for further investigation.

摘要

急性心肌梗死(AMI)给全球带来了沉重的死亡负担。本研究利用生物信息学方法,探索了细胞衰老相关基因(CARGs)和线粒体相关基因(MRGs)在AMI中的作用。使用差异表达分析和加权基因共表达网络分析(WGCNA)对公开的AMI数据集进行分析,以识别1373个差异表达基因(DEGs),其中643个上调,730个下调。通过基因集变异分析(GSVA)确定了一个与细胞衰老相关的蓝绿色模块。维恩分析揭示了37个候选基因,它们是DEGs、关键模块基因和MRGs的交集。机器学习、受试者工作特征(ROC)分析和逆转录定量聚合酶链反应(RT-qPCR)验证了异戊烯基二磷酸δ-异构酶1(IDI1)和佛波酯-12-肉豆蔻酸酯-13-乙酸诱导蛋白1(PMAIP1)是关键的AMI基因。构建了一个全面的lncRNA-miRNA-mRNA网络,环孢素与IDI1(-6.2 kcal/mol)和PMAIP1(-4.8 kcal/mol)表现出很强的结合亲和力,表明其具有治疗潜力。本研究可能为AMI的发病机制提供见解,并突出潜在的药物靶点以供进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/0ed2ba194bf3/41598_2025_5849_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/4c3fac972255/41598_2025_5849_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/a7d17ba1b665/41598_2025_5849_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/7e4fbae49a9b/41598_2025_5849_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/375b007f8eb6/41598_2025_5849_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/169279feb959/41598_2025_5849_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/fd40b210fb3b/41598_2025_5849_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/3772fcac6215/41598_2025_5849_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/0ed2ba194bf3/41598_2025_5849_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/4c3fac972255/41598_2025_5849_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/a7d17ba1b665/41598_2025_5849_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/7e4fbae49a9b/41598_2025_5849_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/375b007f8eb6/41598_2025_5849_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/169279feb959/41598_2025_5849_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/fd40b210fb3b/41598_2025_5849_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/3772fcac6215/41598_2025_5849_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3da1/12216652/0ed2ba194bf3/41598_2025_5849_Fig8_HTML.jpg

相似文献

[1]
Identification of key genes associated with cellular aging and mitochondria in acute myocardial infarction.

Sci Rep. 2025-7-1

[2]
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[3]
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[4]
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[5]
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[6]
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[7]
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[8]
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[9]
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[10]
The role of senescence-related hub genes correlating with immune infiltration in type A aortic dissection: Novel insights based on bioinformatic analysis.

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本文引用的文献

[1]
A transcriptomic analysis of dental pulp stem cell senescence in vitro.

Biomed Eng Online. 2024-10-18

[2]
KEGG: biological systems database as a model of the real world.

Nucleic Acids Res. 2025-1-6

[3]
Identification of mitochondria-related gene biomarkers associated with immune infiltration in acute myocardial infarction.

iScience. 2024-6-14

[4]
Complete Revascularization in Acute Myocardial Infarction: The Clock Is Ticking.

Circ Cardiovasc Interv. 2024-7

[5]
Cellular senescence in normal physiology.

Science. 2024-6-21

[6]
Reperfusion Injury in Patients With Acute Myocardial Infarction: JACC Scientific Statement.

J Am Coll Cardiol. 2024-6-4

[7]
Sodium Glucose Co-Transporter 2 Inhibition Following Acute Myocardial Infarction: The DAPA-MI and EMPACT-MI Trials.

JACC Heart Fail. 2024-5

[8]
JACC Focus Seminar on Mechanical Complications of Acute Myocardial Infarction.

J Am Coll Cardiol. 2024-5-7

[9]
Cellular Senescence, Mitochondrial Dysfunction, and Their Link to Cardiovascular Disease.

Cells. 2024-2-17

[10]
Cannabidiol protects against acute aortic dissection by inhibiting macrophage infiltration and PMAIP1-induced vascular smooth muscle cell apoptosis.

J Mol Cell Cardiol. 2024-4

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