LIMD2 is the Signature of Cell Aging-immune/Inflammation in Acute Myocardial Infarction

Abstract

Background:: Acute 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. background: Acute 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. Methods:: Based 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. Results:: Four 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. Conclusion:: This 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.

DataSheet2.XLSX

“…Aging leads to immune system dysregulations, including Treg cell imbalances in the spleen and fluctuations in CD4 + and CD8 + T cells in the blood. Furthermore, there is an inflammatory response disorder marked by altered levels of IL-6, TNF-α, IL-2, and GDF11 in the serum (Tao et al, 2023). In line with previous research, this study discovered that the anti-aging effects of ginseng included mitigating brain damage through its antioxidant, anti-inflammatory, and immunemodulating properties.…”

DataSheet1.docx

“…Aging leads to immune system dysregulations, including Treg cell imbalances in the spleen and fluctuations in CD4 + and CD8 + T cells in the blood. Furthermore, there is an inflammatory response disorder marked by altered levels of IL-6, TNF-α, IL-2, and GDF11 in the serum (Tao et al, 2023). In line with previous research, this study discovered that the anti-aging effects of ginseng included mitigating brain damage through its antioxidant, anti-inflammatory, and immunemodulating properties.…”

Research on the anti-aging mechanisms of Panax ginseng extract in mice: a gut microbiome and metabolomics approach

“…Aging leads to immune system dysregulations, including Treg cell imbalances in the spleen and fluctuations in CD4 + and CD8 + T cells in the blood. Furthermore, there is an inflammatory response disorder marked by altered levels of IL-6, TNF-α, IL-2, and GDF11 in the serum ( Tao et al, 2023 ). In line with previous research, this study discovered that the anti-aging effects of ginseng included mitigating brain damage through its antioxidant, anti-inflammatory, and immune-modulating properties.…”