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

Area of Science:

• Cardiovascular Biology
• Molecular Medicine
• RNA Biology

Background:

• Acute coronary syndrome (ACS) progression involves atherosclerotic plaque vulnerability.
• Understanding the molecular mechanisms underlying ACS is crucial for developing new therapies.
• Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cardiovascular diseases.

Purpose of the Study:

• To investigate the mechanism of SLC25A25 antisense RNA 1 (SLC25A25-AS1) in the context of ACS.
• To determine the clinical relevance of SLC25A25-AS1 levels in ACS patients.
• To elucidate the regulatory pathway involving SLC25A25-AS1 in response to atherosclerotic stimuli.

Main Methods:

• Serum samples from healthy controls (n=81) and ACS patients (n=162) were analyzed for SLC25A25-AS1 levels using RT-qPCR.
• Correlation, ROC, and logistic regression analyses were performed to assess clinical relevance.
• In vitro experiments using human coronary artery smooth muscle cells (HCASMCs) treated with oxidized low-density lipoprotein (ox-LDL) were conducted to evaluate the functional role of SLC25A25-AS1 and its downstream targets (miR-34a-5p/FOXP1).

Main Results:

• SLC25A25-AS1 was significantly downregulated in ACS patients compared to healthy controls.
• Overexpression of SLC25A25-AS1 demonstrated protective effects against ox-LDL-induced damage in HCASMCs, including reduced abnormal proliferation, inflammation, and cell migration, while maintaining contractile phenotype.
• Bioinformatics and experimental validation confirmed the SLC25A25-AS1/miR-34a-5p/FOXP1 regulatory axis.

Conclusions:

• SLC25A25-AS1 plays a protective role in ACS by mitigating ox-LDL-induced HCASMC dysfunction and inflammation.
• The protective mechanism involves the SLC25A25-AS1/miR-34a-5p/FOXP1 pathway.
• SLC25A25-AS1 may represent a potential therapeutic target for ACS.