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已发表论文
miR-322-5p 在冠心病中的诊断价值及调控机制
Received 6 June 2025
Accepted for publication 16 August 2025
Published 20 September 2025 Volume 2025:18 Pages 13173—13182
DOI https://doi.org/10.2147/JIR.S536945
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Qing Lin
Mingyang Wang,1,* Jing Wang,2,* Yanan Xie3
1Department of Rehabilitation Medicine, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, People’s Republic of China; 2Geriatrics Department, China Aerospace Science & Industry Corporation 731 Hospital, Beijing, People’s Republic of China; 3Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yanan Xie, Department of Cardiology, The Second Hospital of Hebei Medical University, No. 215, Heping West Road, Xinhua District, Shijiazhuang, Hebei, 050000, People’s Republic of China, Tel +86 0311-66003983, Email yananxie15@163.com
Background: Coronary heart disease (CHD) is a heart condition caused by narrowed or blocked coronary arteries. The miR-322-5p is closely related to inflammation and vascular diseases, yet its role in CHD remains unknown.
Objective: This study focused on investigating the clinical significance of miR-322-5p and its regulatory mechanism in CHD.
Materials and Methods: This study enrolled 160 CHD patients and 130 healthy individuals. The expression of miR-322-5p and TRAF6 was measured by RT-qPCR. The correlation between miR-322-5p and CHD was evaluated via Pearson correlation analysis. The clinical predictive performance of miR-322-5p was assessed by ROC analysis. Cell viability was assessed using the CCK-8 assay while apoptosis was analyzed by flow cytometry. Inflammatory cytokine levels were determined by ELISA.
Results: MiR-322-5p was significantly downregulated in patients with CHD and exhibited high diagnostic accuracy for CHD with an AUC of 0.882. The declined miR-322-5p was negatively correlated with Gensini score (r = − 0.611) and CRP (r = − 0.646), but positively associated with HDL-C (r = 0.598). Although miR-322-5p was reduced under pathological conditions, its upregulation enhanced cell viability and inhibited both apoptosis and inflammatory factors. TRAF6, a direct target of miR-322-5p, was negatively regulated by miR-322-5p (r = − 0.683), and high levels of TRAF6 aggravated CHD.
Conclusion: The declined miR-322-5p in CHD presented high diagnostic value. Reduced miR-322-5p exacerbated the CHD by inhibiting cell viability, enhancing apoptosis and inflammation through negatively regulating the TRAF6.
Keywords: miR-322-5p, coronary heart disease, apoptosis, inflammation
1Department of Rehabilitation Medicine, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, People’s Republic of China; 2Geriatrics Department, China Aerospace Science & Industry Corporation 731 Hospital, Beijing, People’s Republic of China; 3Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yanan Xie, Department of Cardiology, The Second Hospital of Hebei Medical University, No. 215, Heping West Road, Xinhua District, Shijiazhuang, Hebei, 050000, People’s Republic of China, Tel +86 0311-66003983, Email yananxie15@163.com
Background: Coronary heart disease (CHD) is a heart condition caused by narrowed or blocked coronary arteries. The miR-322-5p is closely related to inflammation and vascular diseases, yet its role in CHD remains unknown.
Objective: This study focused on investigating the clinical significance of miR-322-5p and its regulatory mechanism in CHD.
Materials and Methods: This study enrolled 160 CHD patients and 130 healthy individuals. The expression of miR-322-5p and TRAF6 was measured by RT-qPCR. The correlation between miR-322-5p and CHD was evaluated via Pearson correlation analysis. The clinical predictive performance of miR-322-5p was assessed by ROC analysis. Cell viability was assessed using the CCK-8 assay while apoptosis was analyzed by flow cytometry. Inflammatory cytokine levels were determined by ELISA.
Results: MiR-322-5p was significantly downregulated in patients with CHD and exhibited high diagnostic accuracy for CHD with an AUC of 0.882. The declined miR-322-5p was negatively correlated with Gensini score (r = − 0.611) and CRP (r = − 0.646), but positively associated with HDL-C (r = 0.598). Although miR-322-5p was reduced under pathological conditions, its upregulation enhanced cell viability and inhibited both apoptosis and inflammatory factors. TRAF6, a direct target of miR-322-5p, was negatively regulated by miR-322-5p (r = − 0.683), and high levels of TRAF6 aggravated CHD.
Conclusion: The declined miR-322-5p in CHD presented high diagnostic value. Reduced miR-322-5p exacerbated the CHD by inhibiting cell viability, enhancing apoptosis and inflammation through negatively regulating the TRAF6.
Keywords: miR-322-5p, coronary heart disease, apoptosis, inflammation