Evaluating the diagnostic potential of SOCS3 in copper metabolism for acute myocardial infarction

Abstract

Acute myocardial infarction (AMI) represents a critical cardiovascular condition necessitating rapid and precise diagnostic strategies. This study investigates the diagnostic implications of genes involved in copper metabolism homeostasis in AMI. We identified genes related to copper metabolism and AMI from Genecards and GEO databases, conducting differential gene analysis via R software. Gene function was annotated through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, while the STRING database facilitated key gene identification via topological analysis. The diagnostic value of these genes, particularly cytokine signaling 3 (SOCS3), was assessed using ROC curve analysis. SOCS3 expression was validated using in-vitro and in-vivo models, including cardiomyocyte hypoxia/reoxygenation (H/R) and rat myocardial infarction (MI) model. Further, we examined the effects of SOCS3 knockout on cell proliferation, apoptosis, and myocardial infarction severity. 77 genes were identified, with 73 showing upregulation and 4 downregulation. These genes mainly participated in pathways related to cytokine activation, inflammation regulation, and lipid metabolism. Network analysis highlighted 10 key genes, with SOCS3 exhibiting significant diagnostic potential (AUC > 0.9). Validation experiments confirmed SOCS3 overexpression in disease models, with its knockout leading to decreased apoptosis, reduced infarct size, and improved cardiac function. This study highlights the diagnostic relevance of genes associated with copper metabolism, particularly SOCS3, in AMI. These findings offer novel insights into the molecular mechanisms of AMI, supporting the development of targeted diagnostic and therapeutic strategies.