Comprehensive analysis of macrophage-associated inflammatory genes in AMI based on bulk combined with single-cell sequencing data.

Background: Previous studies have highlighted the crucial role of macrophages in the post-acute myocardial infarction (AMI) inflammatory response. This study specifically focused on investigating macrophage-related targets involved in the inflammatory response after AMI.

Methods: Bioinformatics methods were applied for identifying differentially expressed genes (DEGs) in datasets GSE163465, GSE236374, and GSE183272 obtained from the Gene Expression Omnibus (GEO) database.

Metabolomic and transcriptomic studies of improvements in myocardial infarction due to Pycr1 deletion.

Myocardial infarction (MI) remains a major challenge to cardiovascular health worldwide, with poor healing leaving a direct impact on patients' quality of life and survival. Metabolic abnormalities after MI are receiving increasing attention. Our previous studies showed that enhancing proline catabolism ameliorates hypoxic damage to myocardial cells; therefore, we sought to determine whether reducing the synthesis of endogenous proline also affects MI.