Senescence-related epicardial adipocyte genes lead to immune infiltration and myocardial infarction progression

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background After coronary artery disease (CAD)-related myocardial injury, reactivation of the epicardium results in cardiac remodeling via paracrine secretion. However, the senescence-related genomic signature that reflects epicardial adipose tissue (EAT) and immune infiltration is not well understood. Methods Adipocyte-related differentially expressed genes (DEGs) were identified in EAT and subcutaneous adipose tissue (SAT) from patients with and without CAD. Immune cells and senescence-related DEGs in EATs were identified. A protein-protein interaction network was used to determine the hub genes. To validate these genes, a Gene Expression Omnibus (GEO) dataset investigation, single cell sequencing analysis and the validation of human sub-epicardial adipose and blood samples were performed. To investigate the mechanism, 3T3-L1 cells were used and differentiated to adipocytes and the hub genes were knocked-down and SASPs were determined. Results A Venn diagram was used to obtain 82 senescence-related DEGs, and the top 15-degree hub genes were explored. After validating using the GEO datasets and human sub-epicardial adipose samples, STAT3, SERPINE1, CDKN2A, DLG4, PTGS2, MDM2, LRP1, IRS2, PRKCD, CCND2 , and CISH were found to be significantly expressed in the group with severe CAD. The hub genes, including STAT3, MDM2, LRP1, IRS2, PRKCD, CCND2 , and CISH , were validated to be h

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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