Uncovering potential molecular markers and pathological mechanisms of Parkinson's disease and myocardial infarction based on bioinformatics analysis

Background The direct association between Parkinson's disease (PD) and Myocardial infarction (MI) has been the subject of relatively limited research. Objective The purpose of this study was to identify the genes most associated with PD and MI to explore their common pathogenesis. Methods The gene expression profiles of PD and MI were downloaded from GEO database. Differential expression analysis was performed to identify the common differential expression genes (DEGs) of PD and MI, followed by functional annotation. Subsequently, protein-protein interaction network were constructed, and hub DEGs were identified based on CytoHubba plugin and LASSO regression analysis. To explore the potential molecular mechanism of hub DEGs, GSEA analysis, immune correlation analysis, drug prediction and molecular docking were performed, and transcription factors (TF) and lncRNA-miRNA-mRNA (ceRNA) regulatory networks were constructed. Results A total of 48 DEGs with the same expression trend were identified in the MI vs. normal control (NC) and PD vs. NC groups. Functional annotation results showed that the common DEGs were significantly enriched in immune and inflammation-related pathways. RPS4Y1 and UTY were the most relevant hub DEGs for PD and MI, and may be involved in the HALLMARK_MYC_TARGETS_V1 and HALLMARK_PROTEIN_SECRETION pathways. TP63 was a common TF of RPS4Y1 and UTY. The PVT1/KCNQ1OT1-hsa-miR-31-5p-RPS4Y1 and KCNQ1OT1-hsa-let-7a-5p/hsa-miR-19b-3p-UTY axes may play an important role in regulating PD and MI. CYCLOHEXIMIDE and ATALAREN may be potential drugs for the treatment of PD and MI comorbidity. In addition, PD and MI exhibit different patterns of immune cell infiltration and immune function status, which may be related to the specific pathological processes of the disease. Conclusions This study revealed for the first time that RPS4Y1 and UTY may be common biomarkers of PD and MI and may be potential therapeutic targets. This study provides new perspective on the common molecular mechanisms between PD and MI.