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Effect of Ghrelin Intervention on the Ras/ERK Pathway in the Regulation of Heart Failure by PTEN
Yong Zhao1, Quan Sun1, Zhenyu Xu2
1Key Laboratory of Microecology-Immune Regulatory Network and Related Diseases, School of Basic Medicine, Jiamusi University, Jiamusi 154007, China.
Objective:
To study the possible mechanism of ghrelin in heart failure and how it works.
Method:
In vitro results demonstrated that ghrelin alleviates cardiac function and reduces myocardial fibrosis in rats with heart failure. Moreover, ghrelin intervention increased PTEN expression level and reduced ERK, c-jun, and c-Fos expression level; in vivo experiments demonstrated that ghrelin intervention reduces mast memory expression and increases cardiomyocyte surface area, PTEN expression level, ERK, c-jun, c-Fos expression level, and cell surface area, while ERK blockade suppresses mast gene expression and reduces cell surface area.
Results:
In vitro experimental results prove that we have successfully constructed a rat model related to heart failure, and ghrelin can alleviate the heart function of heart failure rats and reduce myocardial fibrosis. In addition, ghrelin is closely related to the decrease of the expression levels of ERK, c-jun, and c-Fos, but it can also increase the expression of PTEN in the rat model; in vivo experiments proved that we successfully constructed an in vitro cardiac hypertrophy model, and the intervention of ghrelin would reduce the expression of hypertrophic memory and increase the surface area of cardiomyocytes, increase the expression level of PTEN, and reduce the expression levels of ERK, c-jun, and c-Fos, while the blockade of PTEN will increase the expression of hypertrophy genes and increase the cell surface area, while the blockade of ERK will increase the expression of hypertrophic genes, which in turn will make the cell surface area reducing.
Conclusion:
Ghrelin inhibits the phosphorylation and nuclear entry of ERK by activating PTEN, thereby controlling the transcription of hypertrophic genes, improving myocardial hypertrophy, and enhancing cardiac function.
Insights
Ghrelin improves heart function in heart failure by activating PTEN, which inhibits ERK signaling. This mechanism reduces myocardial hypertrophy and fibrosis, offering a potential therapeutic target for heart conditions.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Heart failure is a complex condition characterized by impaired cardiac function and often associated with myocardial fibrosis and hypertrophy.
- Ghrelin, a peptide hormone, has been investigated for its potential roles in cardiovascular health.
Purpose of the Study:
- To elucidate the mechanism by which ghrelin influences cardiac function in heart failure models.
- To investigate ghrelin's effect on key molecular pathways involved in cardiac remodeling.
Main Methods:
- In vitro and in vivo experiments using rat models of heart failure and cardiac hypertrophy.
- Assessment of cardiac function, myocardial fibrosis, and expression levels of PTEN, ERK, c-jun, and c-Fos.
- Intervention with ghrelin and blockade of PTEN and ERK signaling pathways.
Main Results:
- Ghrelin alleviated cardiac dysfunction and reduced myocardial fibrosis in heart failure models.
- Ghrelin increased PTEN expression and decreased ERK, c-jun, and c-Fos expression.
- Ghrelin intervention in cardiac hypertrophy models increased cardiomyocyte surface area and PTEN expression, while reducing hypertrophic markers.
Conclusions:
- Ghrelin enhances cardiac function by activating PTEN, which subsequently inhibits ERK phosphorylation and nuclear translocation.
- This pathway effectively controls hypertrophic gene transcription, ameliorating myocardial hypertrophy and improving overall cardiac performance.
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