Proteomic insights: the downregulation of serotransferrin and its implications for coronary artery disease

Coronary artery disease (CAD) is a common cardiovascular condition characterised by the narrowing of the coronary arteries due to atherosclerosis, primarily resulting from the accumulation of plaque. It is vital to understand the specific proteins involved in these inflammatory mechanisms to effectively elucidate the pathogenesis of CAD. Additionally, considering the increased prevalence of iron deficiency among individuals with CAD, it is important to identify proteins associated with iron in this context. Isobaric tags for relative and absolute quantification (iTRAQ) were utilised to generate the differential protein profile of CAD plasma. Protein selection was based on peptide similarity and specific fold change criteria, aiming to identify iron transporter proteins. The expression levels of these proteins were subsequently validated using Western blotting and enzyme-linked immunosorbent assay (ELISA). Of the total 197 differentially expressed proteins (DEPs), serotransferrin (TF), an iron transporter, showed downregulation in samples from CAD patients compared to healthy. The cardiac marker troponin I (cTnI) demonstrated an inverse relationship with TF levels. The decreased availability of TF may be attributed to its phosphorylation by calcium/calmodulin-dependent protein kinase (CaMKK2). In silico analyses of TF via GO, KEGG, and Cytoscape show TF is underexplored in CAD. TF protein was significantly associated with CAD progression and inversely correlated with cTnI, suggesting it could be a potential therapeutic target pending further molecular and clinical investigation.