Hes1 is upregulated by ischemic postconditioning and contributes to cardioprotection
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Updated: Apr 20, 2026
A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion
Published on: July 17, 2012
Xue-liang Zhou1, Yong Zhao, Yi-hu Fang
1Department of Cardiac Surgery, The First Affiliated Hospital, Nanchang University, Nanchang, China.
Insights
Hes1 expression increases during ischemic postconditioning, protecting heart cells from damage. This finding suggests Hes1 as a potential therapeutic target for ischemic cardiomyopathy.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Cellular Stress Response
Background:
- Myocardial infarction and ischemic cardiomyopathies elevate Hes1 expression.
- The role of Hes1 in ischemic postconditioning (IPost)-mediated cardioprotection is not well understood.
Purpose of the Study:
- To investigate the function of Hes1 in mediating cardioprotection during IPost.
- To elucidate the molecular mechanisms underlying Hes1-dependent protection.
Main Methods:
- Utilized gain and loss of function approaches in primary cardiac myocytes.
- Exposed cells to ischemia reperfusion injury (IRI) and IPost.
Main Results:
- Hes1 expression was significantly upregulated during IPost.
- Hes1 enhanced cardiomyocyte viability and inhibited apoptosis.
- Hes1 suppressed mitochondrial permeability transition pore (mPTP) opening and reactive oxygen species (ROS) generation.
- Hes1-mediated protection involved downregulation of phosphatase and tensin homolog (PTEN) and activation of PI3K/Akt and STAT3 signaling pathways.
Conclusions:
- Hes1 is upregulated by IPost and plays a crucial role in its cardioprotective effects.
- Hes1 represents a promising therapeutic target for treating ischemic cardiomyopathy.
Abstract:
The expression of Hes1 is increased following myocardial infarct and other ischemic cardiomyopathies, but the role of Hes1 in cardioprotection provided by ischemic postconditioning (IPost) remains unclear. In this study, we used gain and loss of function approaches to investigate the role of Hes1 in cardioprotection during IPost. Primary cardiac myocytes exposed to ischemia reperfusion injury (IRI) and IPost were used as the experimental model. The results showed that Hes1 expression was increased during myocardial IPost, and Hes1 promoted the viability while inhibited the apoptosis of cardiomyocytes. Moreover, Hes1 inhibited the opening of mitochondrial permeability transition pore (mPTP) and the generation of reactive oxygen species in primary cardiac myocytes exposed to IRI. Mechanistically, we found that Hes1-mediated cardioprotection was related to the downregulation of phosphatase and tensin homolog and the activation of phosphatidylinositol 3-kinase/Akt and signal transducer and activator of transcription 3 signalling. These data demonstrate that Hes1 is upregulated and mediates cardioprotection provided by IPost and suggest that Hes1 is a potential new target for the treatment of ischemic cardiomyopathy.
