MicroRNA-663 participates in myocardial fibrosis through interaction with TGF-β1

Xiangyang Wu1, Jie Zhu1, Yalin Wei1

  • 1Department of Cardiac Surgery, The Second Hospital of Lanzhou University, Lanzhou, Gansu 730030, P.R. China.

Insights

MicroRNA-663 (miRNA-663) downregulation is linked to myocardial fibrosis. This study suggests miRNA-663 may protect against fibrosis by regulating transforming growth factor β1 (TGF-β1).

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Fibrosis Research

Background:

  • Myocardial fibrosis is a significant contributor to heart disease.
  • Transforming growth factor β1 (TGF-β1) is implicated in the development of myocardial fibrosis.
  • The role of microRNA-663 (miRNA-663) in myocardial fibrosis is not fully understood.

Purpose of the Study:

  • To investigate the potential role of miRNA-663 in myocardial fibrosis.
  • To determine if miRNA-663 interacts with TGF-β1 in the context of myocardial fibrosis.

Main Methods:

  • Analysis of miRNA-663 and TGF-β1 expression in endomyocardial biopsies from patients with myocardial fibrosis and controls.
  • Pearson's correlation analysis to assess the relationship between miRNA-663 and TGF-β1 levels.
  • Receiver operating characteristic (ROC) curve analysis to evaluate diagnostic potential.
  • In vitro experiments using AC16 human cardiomyocyte cell line to study the effects of miRNA-663 overexpression and TGF-β1 treatment.

Main Results:

  • miRNA-663 expression was significantly downregulated, while TGF-β1 expression was upregulated in myocardial fibrosis patients.
  • A negative correlation was observed between miRNA-663 and TGF-β1 levels in patients with myocardial fibrosis.
  • Downregulation of miRNA-663 effectively distinguished patients with myocardial fibrosis from controls.
  • Overexpression of miRNA-663 in cardiomyocytes reduced TGF-β1 expression, but exogenous TGF-β1 did not affect miRNA-663 levels.

Conclusions:

  • miRNA-663 downregulation is associated with myocardial fibrosis.
  • miRNA-663 may play a protective role in myocardial fibrosis by regulating TGF-β1.
  • The findings suggest a potential therapeutic target for myocardial fibrosis.

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