AI Article Synopsis

  • Coronary artery disease (CAD) is linked to the buildup of atherosclerotic plaques in coronary arteries, driven by the abnormal growth and death of vascular smooth muscle cells (VSMCs).
  • MicroRNA-574-5p (miR-574-5p) levels are significantly increased in patients with CAD, suggesting a connection to disease severity, yet the exact role of miR-574-5p in CAD remains unclear.
  • Research findings indicate that miR-574-5p enhances VSMC proliferation and reduces apoptosis by targeting the ZDHHC14 gene, positioning it as a potential therapeutic target for CAD.

Article Abstract

Coronary artery disease (CAD) is caused by atherosclerotic plaque development in the walls of coronary arteries. Aberrant proliferation of vascular smooth muscle cells (VSMCs) promotes atherosclerotic plaque formation, whereas VSMC apoptosis may promote CAD-related inflammation. microRNAs are potential diagnostic biomarkers in cardiovascular disease, especially CAD. Previous reports found that, among patients with CAD, microRNA-574-5p (miR-574-5p) expression was significantly increased and associated with disease severity. However, the specific mechanism by which miR-574-5p affects CAD is unknown. We used quantitative real-time PCR to detect the mRNA expression levels of miR-574-5p in the sera and VSMCs of patients with CAD. We also detected cell proliferation by MTT assay and apoptosis by the Cell Death Detection ELISA-Plus apoptosis assay. We found that miR-574-5p expression was elevated in the sera and VSMCs of patients with CAD. Additionally, miR-574-5p overexpression promoted cell proliferation and inhibited apoptosis in VSMCs. A dual-luciferase reporter assay showed that miR-574-5p directly targets ZDHHC14. In conclusion, our findings indicate that miR-574-5p promotes cell proliferation and inhibits apoptosis by inhibiting ZDHHC14 gene expression, suggesting that miR-574-5p is a CAD-related factor that may serve as a potential molecular target for CAD treatment.

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Source
http://dx.doi.org/10.1016/j.biopha.2017.10.062DOI Listing

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