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Updated: Jun 3, 2025
Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
Pericarpium Trichosanthis Inhibits TGF-β1-Smad3 Pathway-Induced Cardiac Fibrosis in Heart Failure Rats via
Yue He1, Meng-Shi Dai2, Li-Yu Tao3
1Shanghai University of Traditional Chinese Medicine, Shanghai Eighth People's Hospital, Shanghai, China.
Insights
Pericarpium Trichosanthis (PT) effectively treats cardiac fibrosis and dysfunction in chronic heart failure (CHF) by modulating the TGF-β/Smad3 pathway and miR-29b expression, offering new therapeutic potential.
Area of Science:
- Cardiovascular Biology
- Pharmacology
- Molecular Medicine
Background:
- Cardiac fibrosis is a key contributor to chronic heart failure (CHF) pathogenesis.
- The precise molecular pathways driving cardiac fibrosis in CHF are not fully understood.
- Pericarpium Trichosanthis (PT) has shown potential in treating fibrotic diseases.
Purpose of the Study:
- To investigate the therapeutic effects of Pericarpium Trichosanthis (PT) on cardiac fibrosis in a rat model of chronic heart failure (CHF).
- To elucidate the underlying molecular mechanisms of PT's action, focusing on the TGF-β/Smad3 signaling pathway and miR-29b.
Main Methods:
- Cardiac fibrosis was induced in rats via left anterior descending (LAD) coronary artery ligation.
- In vivo studies assessed myocardial fibrosis, cardiac activity, TGF-β1 levels, and miR-29b expression following PT treatment.
- In vitro experiments utilized cardiac fibroblasts stimulated with TGF-β1 to evaluate PT's effects on fibroblast activation, collagen synthesis, TGF-β1, and miR-29b.
Main Results:
- PT treatment significantly reduced myocardial fibrosis and improved cardiac activity in CHF rats.
- PT administration led to decreased TGF-β1 levels and increased miR-29b expression in vivo and in vitro.
- PT suppressed TGF-β1-induced fibroblast activation and collagen synthesis, acting via the TGF-β/Smad3 pathway.
- miR-29b was found to suppress TGF-β1 expression, and its inhibition attenuated PT's anti-fibrotic effects.
Conclusions:
- Pericarpium Trichosanthis (PT) demonstrates significant therapeutic potential for cardiac fibrosis and dysfunction in chronic heart failure (CHF).
- PT exerts its beneficial effects by modulating the TGF-β/Smad3 signaling pathway and influencing miR-29b expression.
- The findings suggest a novel therapeutic strategy for CHF involving PT and its interaction with the miR-29b/TGF-β1 axis.
Abstract:
Cardiac dysfunction and adverse consequences induced by cardiac fibrosis have been well documented. However, the cardiac fibrosis pathway in chronic heart failure (CHF) remains unclear, and it is therefore necessary to conduct further research for the sake of developing more effective therapeutic strategies for CHF. Some recent studies suggest that Pericarpium Trichosanthis (PT) may help improve the progression of fibrotic diseases. To validate this possibility, we conducted an experiment to evaluate the effect of PT on cardiac fibrosis and explore the hidden mechanism. In the experiment, we induced cardiac fibrosis in rats by left anterior descending (LAD) coronary artery ligation. The findings revealed that PT reduced myocardial fibrosis and increased cardiac activity in CHF rats receiving LAD ligation. In addition, the TGF-β1 level was decreased, and the miR-29b expression was increased in CHF rats after PT treatment. Our in vitro experiment also demonstrated that PT treatment suppressed fibroblast activation and collagen synthesis in cardiac fibroblasts stimulated by TGF-β1， and at the same time decreased the TGF-β1 level and increased the miR-29b expression. We further verified that this action was correlated with the TGF-β/Smad3 signaling pathway. We also observe that miR-29b could suppress the TGF-β1 expression, and the suppression of miR-29b weakened the anti-fibrotic effect of PT. This suggests that PT could cure cardiac fibrosis and dysfunction both in vitro and in vivo via the TGF-β/Smad3 signaling pathway, while miR-29b may participate in this action.
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