Up-regulated lncRNA SNHG9 mediates the pathogenesis of dilated cardiomyopathy via miR-326/EPHB3 axis

Fan Zhang1,2, Hongtao Shi1, Honghong Xue2

  • 1Department of Cardiology, the First Hospital of Shanxi Medical University, 85 South Jiefang Road, Taiyuan, Shanxi Province, 030001, People's Republic of China.

Insights

Serum SNHG9, a long non-coding RNA, acts as a promising biomarker for dilated cardiomyopathy (DCM). Its levels effectively distinguish DCM patients and correlate with heart function, suggesting a regulatory role in disease development.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Biomarker Discovery

Background:

  • Dilated cardiomyopathy (DCM) is a primary cause of heart failure and a leading reason for heart transplantation.
  • Long non-coding RNAs (lncRNAs) are implicated in cardiac disease pathogenesis, but their specific roles in DCM remain unclear.

Purpose of the Study:

  • To investigate the potential of serum lncRNAs as biomarkers for DCM.
  • To identify specific lncRNAs, such as SNHG9, involved in DCM development and progression.

Main Methods:

  • Re-analysis of GEO dataset (GSE124405) to identify aberrant plasma lncRNAs in heart failure patients.
  • Utilized Receiver Operating Characteristic (ROC) curve analysis to evaluate the diagnostic performance of lncRNAs, including SNHG9.
  • Assessed serum SNHG9 expression in a doxorubicin-induced DCM mouse model and evaluated the effect of SNHG9 deletion.

Main Results:

  • Serum SNHG9 demonstrated significant diagnostic capability in distinguishing DCM from healthy controls and differentiating between DCM stages.
  • Upregulated serum SNHG9 levels in a DCM mouse model were negatively correlated with cardiac function.
  • AAV-9 mediated deletion of SNHG9 ameliorated cardiac injury in the doxorubicin-induced DCM model.

Conclusions:

  • Serum SNHG9 is identified as a novel and valuable biomarker for dilated cardiomyopathy.
  • SNHG9 plays a regulatory role in the development and progression of DCM.
  • Targeting SNHG9 may offer a potential therapeutic strategy for DCM.

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