ArticleExperimental and therapeutic medicine2019
MicroRNA-663 participates in myocardial fibrosis through interaction with TGF-β1.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Mechanism of action of non-coding RNAs and traditional Chinese medicine in myocardial fibrosis: Focus on the TGF-β/Smad signaling pathway.Frontiers in pharmacology · 2023Review
- New Insights into the Functions of MicroRNAs in Cardiac Fibrosis: From Mechanisms to Therapeutic Strategies.Genes · 2022Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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