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Objectives <p>Pro-inflammatory molecules are key risk factors for coronary artery diseases (CAD). Therefore, the regulation of inflammatory responses plays a crucial role in CAD. Suppressor of cytokine signaling 4 (SOCS4) is a negative regulator of cytokine signaling may significantly contribute to the pathogenesis of CAD. Bioinformatics studies indicate that hsa-miR-568-5p can target SOCS4. This study aimed to evaluate the expression of hsa-miR-568-5p in patients with CAD and investigate its correlation with SOCS4 levels.</p> Methods <p>The study included 20 Iranian participants without artery stenosis and 40 with artery stenosis. The relative expression levels of hsa-miR-568-5p and SOCS4 were assessed using Real-Time PCR.</p> Results <p>The findings revealed no significant difference in the expression levels of hsa-miR-568-5p and SOCS4 between the two groups. Also, correlations were not observed between hsa-miR-568-5p, SOCS4, and age in both the control and CAD patient groups.</p> Conclusions <p>While hsa-miR-568-5p regulates SOCS4 expression, and SOCS4 upregulation is implicated in coronary artery disease (CAD) protection, this study found no conclusive evidence supporting this relationship. Further research is warranted.</p>

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MiR-568-5p, the key regulator of suppressor of cytokine signaling 4 (SOCS4) in the coronary artery disease

  • 期刊论文

  • 发表日期：

    2025年4月22日

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  • Tayebeh Sadeghi,
  • Majid Zaki-Dizaji,
  • Meisam Rostaminasab Dolatabad,
  • Zahra Taheri

摘要

Objectives

Pro-inflammatory molecules are key risk factors for coronary artery diseases (CAD). Therefore, the regulation of inflammatory responses plays a crucial role in CAD. Suppressor of cytokine signaling 4 (SOCS4) is a negative regulator of cytokine signaling may significantly contribute to the pathogenesis of CAD. Bioinformatics studies indicate that hsa-miR-568-5p can target SOCS4. This study aimed to evaluate the expression of hsa-miR-568-5p in patients with CAD and investigate its correlation with SOCS4 levels.

Methods

The study included 20 Iranian participants without artery stenosis and 40 with artery stenosis. The relative expression levels of hsa-miR-568-5p and SOCS4 were assessed using Real-Time PCR.

Results

The findings revealed no significant difference in the expression levels of hsa-miR-568-5p and SOCS4 between the two groups. Also, correlations were not observed between hsa-miR-568-5p, SOCS4, and age in both the control and CAD patient groups.

Conclusions

While hsa-miR-568-5p regulates SOCS4 expression, and SOCS4 upregulation is implicated in coronary artery disease (CAD) protection, this study found no conclusive evidence supporting this relationship. Further research is warranted.