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Updated: Jan 23, 2026

Tachycardia-Induced Cardiomyopathy As a Chronic Heart Failure Model in Swine
Published on: February 17, 2018
LncRNA GASL1 is downregulated in chronic heart failure and regulates cardiomyocyte apoptosis
Haihong Deng1, Wenbo Ouyang1, Li Zhang2
11Department of Anesthesiology, The First People's Hospital of Zhaoqing, Zhaoqing City, Guangdong Province 526000 People's Republic of China.
Insights
Long non-coding RNA GASL1 is downregulated in chronic heart failure (CHF). Overexpressing GASL1 may improve CHF by reducing heart cell apoptosis via TGF-β1 inactivation.
Area of Science:
- Cardiology
- Molecular Biology
- Genetics
Background:
- Transforming growth factor-beta 1 (TGF-β1) is implicated in chronic heart failure (CHF).
- Long non-coding RNA GASL1 is known to inactivate TGF-β1 in cancer biology.
Purpose of the Study:
- To investigate the role of lncRNA GASL1 in chronic heart failure.
- To explore the relationship between GASL1, TGF-β1, and cardiomyocyte apoptosis in CHF.
Main Methods:
- Plasma samples from CHF patients and controls were analyzed using ELISA and RT-qPCR.
- Cardiomyocyte experiments involved vectors, transient transfections, and western blot.
- Cellular apoptosis was assessed under H2O2 treatment.
Main Results:
- CHF patients exhibited higher plasma TGF-β1 and lower GASL1 levels.
- GASL1 and TGF-β1 were inversely correlated in CHF patients.
- GASL1 overexpression downregulated TGF-β1 in cardiomyocytes and reduced apoptosis, while TGF-β1 overexpression increased apoptosis.
Conclusions:
- GASL1 is downregulated in CHF.
- GASL1 overexpression demonstrates potential therapeutic benefits for CHF by inhibiting cardiomyocyte apoptosis through TGF-β1 inactivation.
Background:
TGF-β1 contributes to chronic heart failure. It is known that lncRNA GASL1 can inactivate TGF-β1 in cancer biology.
Methods:
All the participants were enrolled in the First People's Hospital of Zhaoqing during the period June 2012 to June 2013. ELISA, RT-qPCR, vectors, transient transfections and western blot were carried out during the research.
Results:
We found that plasma levels of TGF-β1 were significantly higher, while levels of GASL1 in plasma were significantly lower in chronic heart failure (CHF) patients compared to the control group. TGF-β1 and GASL1 were inversely correlated in CHF patients. Low pretreatment plasma levels of GASL1 were closely associated with poor survival of CHF patients. GASL1 expression was not significantly affected by TGF-β1 overexpression in cardiomyocytes, while cardiomyocytes with GASL1 overexpression showed downregulated TGF-β1. Overexpression of GASL1 led to a decreased, while TGF-β1 overexpression led to an increased apoptotic rate of cardiomyocytes under H2O2 treatment. In addition, TGF-β1 overexpression attenuated the effect of GASL1 overexpression.
Conclusion:
In conclusion, GASL1 was downregulated in CHF. GASL1 overexpression may improve CHF by inhibiting cardiomyocyte apoptosis through the inactivation of TGF-β1.
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