Exploring the Potential Role of SLC25A25-AS1 in Acute Coronary Syndrome

The progression of acute coronary syndrome (ACS) is primarily determined by the transition from stable to vulnerable atherosclerotic plaque. The primary objective of this study was to investigate the mechanism of SLC25A25 antisense RNA 1 (SLC25A25-AS1) in ACS. The level of SLC25A25-AS1 was determined using reverse transcription quantitative real-time PCR (RT-qPCR) in serum samples from healthy controls (n = 81) and ACS patients (n = 162). The clinical relevance of SLC25A25-AS1 in ACS was evaluated through correlation, receiver operating characteristic (ROC), and logistic regression analyses. SLC25A25-AS1 was significantly downregulated in ACS patients. Overexpression of SLC25A25-AS1 protected oxidized low-density lipoprotein (ox-LDL) treated human coronary artery smooth muscle cells (HCASMCs) from damage in an in vitro atherosclerosis model. Specifically, these protective effects were against abnormal cell proliferation, inflammatory responses, cell migration, and maintenance of the contractile phenotype in HCASMCs. Both bioinformatics analyses and experimental validation confirmed the existence of the SLC25A25-AS1/ microRNA‑34a‑5p (miR-34a-5p)/Forkhead box P1 (FOXP1) regulatory axis. Collectively, SLC25A25-AS1 modulated ox-LDL-induced atherosclerotic responses in HCASMCs through the miR-34a-5p/FOXP1 pathway. These findings suggested that SLC25A25-AS1 may play a protective role in ACS by alleviating ox-LDL-induced HCASMC dysfunction and inflammation via the miR-34a-5p/FOXP1 axis.