Related Experiment Video
Updated: Jan 6, 2026

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
Published on: August 3, 2018
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.
Abstract:
MicroRNA-663 (miRNA-663) regulates the expression of transforming growth factor β1 (TGF-β1), which participates in the pathogenesis of myocardial fibrosis. Therefore, microRNA-663 may also serve a role in myocardial fibrosis. The present study aimed to determine whether miRNA-663 participates in myocardial fibrosis via interaction with TGF-β1. In the present study, the expression of miRNA-663 was significantly downregulated, whereas that of TGF-β1 was significantly upregulated in the endomyocardial biopsies of patients with myocardial fibrosis compared with those in control necropsies. Pearson's correlation analysis revealed that the expression levels of miRNA-663 were negatively correlated with those of TGF-β1 in patients with myocardial fibrosis, but not in the controls. Receiver operating characteristic curve analysis demonstrated that the downregulation of miRNA-663 distinguished patients with myocardial fibrosis from controls. In the AC16 human cardiomyocyte cell line, miRNA-663 overexpression resulted in downregulated TGF-β1 expression, whereas exogenous TGF-β1 treatment exhibited no significant effects on miRNA-663 expression. These results indicate that miRNA-663 may participate in myocardial fibrosis, possibly through interaction with TGF-β1.
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.
Related Concept Videos
TGF - β Signaling Pathway
MicroRNAs
MicroRNAs
Myocarditis I: Introduction

