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pmid:39069811

Energy Metabolism Dysregulation in Myocardial Infarction: An Integrative Analysis of Ischemic Cardiomyopathy.

Zongtao Wang · Zhixin Xie · Tudi Li · Rong Chen · Zhihuan Zeng · Jun Guo

Current vascular pharmacology · 2025 doi:10.2174/0115701611289159240724114844

Paper

complete

Experiment

complete

Data

partial

Analysis

complete

Execution

absent

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Record details sci_version · id · kind · revision · content_hash · schema · created_at · updated_at · generator
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pmid:39069811
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science-record
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title
Energy Metabolism Dysregulation in Myocardial Infarction: An Integrative Analysis of Ischemic Cardiomyopathy.
doi
10.2174/0115701611289159240724114844
pmid
39069811
authors array · 6 items
[0]
Zongtao Wang
[1]
Zhixin Xie
[2]
Tudi Li
[3]
Rong Chen
[4]
Zhihuan Zeng
[5]
Jun Guo
journal
Current vascular pharmacology
year
2025
abstract
BACKGROUND: Myocardial metabolism is closely related to functional changes after myocardial infarction (MI). OBJECTIVE: This study aimed to present an integrative examination of human ischemic cardiomyopathy. METHODS: We used both GSE121893 single-cell suspension sequencing and GSE19303 transcription microarray data sets from the GEO database, along with a murine MI model for full-spectrum metabolite detection. Through a systematic investigation that involved differential metabolite identification and functional enrichment analysis, we shed light on the pivotal role of energy metabolism dysregulation in the progression of MI. RESULTS: Our findings revealed an association between the core regulatory genes CDKN1A, FOS, ITGB4, and MAP2K1 and the underlying pathophysiology of the disease. These genes are identified as critical elements in the complex landscape of myocardial ischemic disorder, highlighting novel insights into therapeutic targets and the intricate biological mechanisms involved. CONCLUSION: This analysis provides a framework for future research on the metabolic alterations associated with MI.
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The differentially expressed genes (DEGs) were identified using standard methods, such as the DESeq2 package or edgeR package in R, based on criteria with B-H adjusted p-value < 0.05 and log2|fold-change| more than 0.25.
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sections[6] "Clustering and Identification of Marker Genes" paragraph 2
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The differentially expressed genes (DEGs) were identified using standard methods, such as the DESeq2 package or edgeR package in R, based on criteria with B-H adjusted p-value < 0.05 and log2|fold-change| more than 0.25.
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All the data and supporting information are provided within the article.
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The study identified CDKN1A, FOS, ITGB4, and MAP2K1 as core regulatory genes associated with energy metabolism dysregulation and the pathophysiology of myocardial infarction.
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Our findings revealed an association between the core regulatory genes CDKN1A, FOS, ITGB4, and MAP2K1 and the underlying pathophysiology of the disease.
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Dissecting cell composition and cell-cell interaction network of human disease heart tissue by single-cell sequencing
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Changes of myocardial gene expression and protein composition in patients with dilated cardiomyopathy after immunoadsorption with subsequent immunoglobulin substitution
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Through a systematic investigation that involved differential metabolite identification and functional enrichment analysis, we shed light on the pivotal role of energy metabolism dysregulation in the progression of MI.\nRESULTS: Our findings revealed an association between the core regulatory genes CDKN1A, FOS, ITGB4, and MAP2K1 and the underlying pathophysiology of the disease. 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