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Peer-reviewedCC BY-NC-NDJournal of cardiothoracic surgery

Value of lncRNA SNHG1 targeted regulation of miR-16-5p in diagnosis and prognosis of patients with aortic dissection.

  • Jiangang Guo1
  • Zhida Yin2
  • Zunrong Liu2
  • Yunjie Hu3
  1. 1Department of Vascular Intervention, The First Affiliated Hospital of Guilin Medical University, Guilin, 541001, Guangxi, China.
  2. 2Department of Interventional vascular surgery, Mindong Hospital Affiliated to Fujian Medical University, Fuan, 355000, Fujian, China.
  3. 3Department of Cardiovascular Surgery, The Affiliated Hospital of Shandong Second Medical University, Weifang, Shandong, China. [email protected].
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Abstract

Background

Aortic dissection (AD) is a critical macrovascular emergency related to the morphology of vascular smooth muscle cell (VSMC). LncRNA SNHG1 is abnormally expressed in AD patients, but its specific mechanism and prognostic value remain unclear. This study investigated lncRNA SNHG1 expression, diagnostic and prognostic value in AD.Methods

RT-qPCR detected lncRNA SNHG1 expression in AD patients. ROC evaluated diagnostic value. Kaplan-Meier curve and Cox Proportional Hazards Regression Model analyzed prognostic value. Cell counting kit 8 (CCK-8) determined cell activity, flow cytometry measured apoptosis, and luciferase reporter gene analysis identified lncRNA SNHG1-miR-16-5p targeting.Results

LncRNA SNHG1 expression in AD patients was clearly lower than that in controls (P < 0.001), and negatively correlated with AD risk score. LncRNA SNHG1 exhibited diagnostic and prognostic value in AD. In vitro, overexpression of lncRNA SNHG1 promoted VSMCs proliferation and inhibited apoptosis. Luciferase reporter genes showed that lncRNA SNHG1 directly targeted miR-16-5p, with negative correlation. Up-regulation of miR-16-5p reversed the pro-proliferative and anti-apoptotic effects of lncRNA SNHG1.Conclusions

LncRNA SNHG1 may participate in the pathogenesis of AD by targeting miR-16-5p and become a potential diagnostic biomarker for AD.

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Cite

BibTeXRIS
BibTeX
@article{guo2026value,
  title = {{Value of lncRNA SNHG1 targeted regulation of miR-16-5p in diagnosis and prognosis of patients with aortic dissection.}},
  author = {Jiangang Guo and Zhida Yin and Zunrong Liu and Yunjie Hu},
  journal = {Journal of cardiothoracic surgery},
  year = {2026},
  month = aug,
  doi = {10.1186/s13019-026-04645-1},
  url = {https://europepmc.org/article/MED/42968114},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Value of lncRNA SNHG1 targeted regulation of miR-16-5p in diagnosis and prognosis of patients with aortic dissection.
AU  - Jiangang Guo
AU  - Zhida Yin
AU  - Zunrong Liu
AU  - Yunjie Hu
PY  - 2026
DA  - 2026/08/05
JO  - Journal of cardiothoracic surgery
DO  - 10.1186/s13019-026-04645-1
UR  - https://europepmc.org/article/MED/42968114
AB  - Background  Aortic dissection (AD) is a critical macrovascular emergency related to the morphology of vascular smooth muscle cell (VSMC). LncRNA SNHG1 is abnormally expressed in AD patients, but its specific mechanism and prognostic value remain unclear. This study investigated lncRNA SNHG1 expression, diagnostic and prognostic value in AD.Methods  RT-qPCR detected lncRNA SNHG1 expression in AD patients. ROC evaluated diagnostic value. Kaplan-Meier curve and Cox Proportional Hazards Regression Model analyzed prognostic value. Cell counting kit 8 (CCK-8) determined cell activity, flow cytometry measured apoptosis, and luciferase reporter gene analysis identified lncRNA SNHG1-miR-16-5p targeting.Results  LncRNA SNHG1 expression in AD patients was clearly lower than that in controls (P < 0.001), and negatively correlated with AD risk score. LncRNA SNHG1 exhibited diagnostic and prognostic value in AD. In vitro, overexpression of lncRNA SNHG1 promoted VSMCs proliferation and inhibited apoptosis. Luciferase reporter genes showed that lncRNA SNHG1 directly targeted miR-16-5p, with negative correlation. Up-regulation of miR-16-5p reversed the pro-proliferative and anti-apoptotic effects of lncRNA SNHG1.Conclusions  LncRNA SNHG1 may participate in the pathogenesis of AD by targeting miR-16-5p and become a potential diagnostic biomarker for AD.
SN  - 1749-8090
ER  -