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Background <p>Asymptomatic carotid artery stenosis (ACAS) results in a delayed diagnosis and thereafter increases the risk of an individual experiencing a cerebrovascular event. The current study has assessed the expression of miR-654-3p in patients with ACAS and determined its clinical relevance. Further, the study aimed to investigate whether miR-654-3p could regulate inflammation related to carotid artery stenosis (CAS) by interacting with Forkhead box O1 (FOXO1).</p> Methods <p>115 patients with ACAS and 110 healthy controls were recruited to this study. qRT-PCR was performed for the expression levels of miR-654-3p and FOXO1. To mimic the in vitro conditions of the pathophysiology of CAS, human aortic endothelial cells (HAECs) were incubated with oxidized low-density lipoprotein&#xa0;(ox-LDL). The CCK-8 kit assays were used to evaluate cell viability, Transwell assays were used to evaluate migratory capacity, and flow cytometry was employed to determine the rate of apoptosis. Additionally, the inflammatory mediators’ contents: ICAM-1, VCAM-1, MCP-1, TNFα, and IL-6 were measured using ELISA. Direct interactions between miR-654-3p and FOXO1 were validated by dual-luciferase reporter assays.</p> Results <p>Patients with ACAS express lower levels of miR-654-3p, which better predict diagnostic and prognostic possibilities. In functional studies, we demonstrated that transfection with miR-654-3p mimics promotes cell proliferation and migration in HAECs treated with ox-LDL while reducing the proportion of the apoptotic population. Moreover, increased secretion of ICAM-1, VCAM-1, MCP-1, TNFα, and IL-6 brands the ox-LDL-induced inflammatory response, all of which were reduced with miR-654-3p overexpression. Conversely, FOXO1 overexpression antagonized the protective effects of miR-654-3p upregulation in HAECs.</p> Conclusion <p>miR-654-3p may serve as a clinical diagnostic and prognostic marker for CAS. In vitro experiments confirm that miR-654-3p may regulate the function and inflammatory response of HAECs by targeting FOXO1, providing new molecular insights into the pathophysiological process of ACAS.</p>

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Research on the role of miR-654-3p as a diagnostic marker for patients with carotid artery stenosis and in predicting the occurrence of cerebral ischemic events

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月20日

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  • Qi Zhang,
  • Zeyu Li,
  • Yanjiang Li,
  • Lijuan Liu,
  • Ke Li

摘要

Background

Asymptomatic carotid artery stenosis (ACAS) results in a delayed diagnosis and thereafter increases the risk of an individual experiencing a cerebrovascular event. The current study has assessed the expression of miR-654-3p in patients with ACAS and determined its clinical relevance. Further, the study aimed to investigate whether miR-654-3p could regulate inflammation related to carotid artery stenosis (CAS) by interacting with Forkhead box O1 (FOXO1).

Methods

115 patients with ACAS and 110 healthy controls were recruited to this study. qRT-PCR was performed for the expression levels of miR-654-3p and FOXO1. To mimic the in vitro conditions of the pathophysiology of CAS, human aortic endothelial cells (HAECs) were incubated with oxidized low-density lipoprotein (ox-LDL). The CCK-8 kit assays were used to evaluate cell viability, Transwell assays were used to evaluate migratory capacity, and flow cytometry was employed to determine the rate of apoptosis. Additionally, the inflammatory mediators’ contents: ICAM-1, VCAM-1, MCP-1, TNFα, and IL-6 were measured using ELISA. Direct interactions between miR-654-3p and FOXO1 were validated by dual-luciferase reporter assays.

Results

Patients with ACAS express lower levels of miR-654-3p, which better predict diagnostic and prognostic possibilities. In functional studies, we demonstrated that transfection with miR-654-3p mimics promotes cell proliferation and migration in HAECs treated with ox-LDL while reducing the proportion of the apoptotic population. Moreover, increased secretion of ICAM-1, VCAM-1, MCP-1, TNFα, and IL-6 brands the ox-LDL-induced inflammatory response, all of which were reduced with miR-654-3p overexpression. Conversely, FOXO1 overexpression antagonized the protective effects of miR-654-3p upregulation in HAECs.

Conclusion

miR-654-3p may serve as a clinical diagnostic and prognostic marker for CAS. In vitro experiments confirm that miR-654-3p may regulate the function and inflammatory response of HAECs by targeting FOXO1, providing new molecular insights into the pathophysiological process of ACAS.