ArticleCurrent medicinal chemistry2024
LIMD2 is the Signature of Cell Aging-immune/Inflammation in Acute Myocardial Infarction.
Article in Current medicinal chemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- High Mobility Group Protein B1 Mediates the Role of the Neutrophil Extracellular Traps in the Progression of Acute Myocardial Infarction.Cardiovascular drugs and therapy · 2026Article
- Cellular and molecular mechanisms underlying cardiovascular aging.Cellular & molecular biology letters · 2025Review
- Elucidating the Neuroprotective Mechanisms of G-3702 in Ischemic Stroke via Integrated Metabolomics and Computational Approaches.CNS neuroscience & therapeutics · 2025Article
- Patterns among factors associated with myocardial infarction: chi-squared automatic interaction detection tree and binary logit model.BMC public health · 2025Article
- Research on biliary atresia and epigenetic factors from the perspective of transcriptomics: identification of key genes and experimental validation.Frontiers in pediatrics · 2025Article
- Identification and validation of key genes associated with cell senescence in acute myocardial infarction.Frontiers in cardiovascular medicine · 2025Article
- Research on the anti-aging mechanisms ofFrontiers in pharmacology · 2024Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundAcute myocardial infarction (AMI) is an age-dependent cardiovascular disease in which cell aging, immunity, and inflammatory factors alter the course; however, cell aging-immune/inflammation signatures in AMI have not been investigated.
methodsBased on the GEO database to obtain microRNA (miRNA) sequencing, mRNA sequencing and single-cell sequencing data, and utilizing the Seurat package to identify AMI-associated cellular subpopulations. Subsequently, differentially expressed miRNAs and mRNAs were screened to establish a network of competing endogenous RNAs (ceRNAs). Senescence and immunity scores were calculated by single sample gene set enrichment analysis (ssGSEA), ESTIMATE and CIBERSORT algorithms, and the Hmisc package was used to screen for genes with the highest correlation with senescence and immunity scores. Finally, protein-protein interaction (PPI) and molecular docking analyses were performed to predict potential therapeutic agents for the treatment of AMI.
resultsFour cell types (Macrophage, Fibroblast, Endothelial cells, CD8 T cells) were identified in AMI, and CD8 T cells exhibited the lowest cell aging activity. A ceRNA network of miRNAs- mNRA interactions was established based on the overlapping genes in differentially expressed miRNAs (DEmiRNAs) target genes and differentially expressed mRNAs (DEmRNAs). Twenty-four marker genes of CD8 T cells were observed. LIMD2 was identified as cell aging- immune/inflammation-related hub gene in AMI. This study also identified a potential therapeutic network of DB03276-LIMD2-AMI, which showed excellent and stable binding status between DB03276-LIMD2.
conclusionThis study identified LIMD2 as a cell aging-immune/inflammation-related hub gene. The understanding of the pathogenesis and therapeutic mechanisms of AMI was enriched by the ceRNA network and DB03276-LIMD2-LAMI therapeutic network.
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