ArticleScientific reports2025
Identification of key genes associated with cellular aging and mitochondria in acute myocardial infarction.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Inhibiting the Hif-1α-Drp1 axis alleviates mitochondrial dysfunction and reduces senescence-like changes in myocardial tissue after acute myocardial infarction.Biology direct · 2026Article
- SASP-mediated cellular senescence following myocardial infarction: from spatiotemporal immune regulation to therapeutic strategies.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
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.
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Registered trials
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