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Updated: Feb 28, 2026
In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
Shock Wave Therapy Promotes Cardiomyocyte Autophagy and Survival during Hypoxia
Insights
Cardiac shock wave therapy (CSWT) promotes cardiomyocyte autophagy during hypoxia. This therapy enhances cell viability and function by modulating the AMPK/mTOR pathway, offering a potential treatment for ischemic heart disease.
Area of Science:
- Cardiovascular Research
- Cellular Biology
- Biomedical Engineering
Background:
- Autophagy's role in cardiovascular disease is debated, particularly in hypoxic myocardium.
- Cardiac shock wave therapy (CSWT) shows promise for ischemic heart disease.
- The effect of CSWT on cardiomyocyte autophagy under hypoxia remains unclear.
Purpose of the Study:
- To investigate the impact of CSWT on cardiomyocyte autophagy in a myocardial hypoxia model.
- To evaluate the potential of CSWT to regulate autophagy and protect cardiomyocytes during hypoxia.
Main Methods:
- H9c2 cells were subjected to hypoxia and treated with varying energies of shock waves (SWs).
- Cell viability, intracellular ATP levels, and autophagic vacuoles were assessed.
- Key proteins involved in autophagy and hypoxia signaling (LC3B, AMPK, mTOR, Beclin-1, Sirt1, HIF-1α) were analyzed via Western blot.
Main Results:
- Hypoxia decreased cardiomyocyte viability and ATP levels while increasing autophagy.
- SW treatment (0.05 mJ/mm2) significantly improved cell viability, ATP levels, and autophagic activity.
- SWs modulated key signaling pathways, increasing p-AMPK and Sirt1, and decreasing p-mTOR and HIF-1α.
Conclusions:
- CSWT shows potential to enhance cardiomyocyte autophagy under hypoxic conditions.
- The protective effects of CSWT may be mediated through the regulation of the AMPK/mTOR signaling pathway.
- CSWT could be a novel therapeutic strategy for hypoxic myocardial injury.
Background:
Autophagy plays an important role in cardiovascular disease. Controversy still exists regarding the effect of autophagy on ischemic/hypoxic myocardium. Cardiac shock wave therapy (CSWT) is an effective alternative treatment for refractory ischemic heart disease. Whether CSWT can regulate cardiomyocyte autophagy under hypoxic conditions is not clear. We established a myocardial hypoxia model using the H9c2 cell line and performed shock waves (SWs) treatment to evaluate the effect of SW on autophagy.
Methods:
The H9c2 cells were incubated under hypoxic conditions, and SW treatment was then performed at energies of 0.02, 0.05, or 0.10 mJ/mm2. The cell viability and intracellular ATP level were examined. Western blot analysis was used to assess the expression of LC3B, AMPK, mTOR, Beclin-1, Sirt1, and HIF-1α. Autophagic vacuoles were visualized by monodansylcadaverine staining.
Results:
After the 24-hour hypoxic period, cardiomyocyte viability and ATP levels were decreased and autophagy was significantly increased in H9c2 cells. SW treatment with an energy of 0.05 mJ/mm2 significantly increased the cellular viability, ATP level, LC3B-II/I, and number of autophagic vacuoles. In addition, phosphorylated AMPK and Sirt1 were increased and phosphorylated mTOR and HIF-1α were decreased after SW treatment.
Conclusion:
SW treatment can potentially promote cardiomyocyte autophagy during hypoxia and protect cardiomyocyte function by regulating the AMPK/mTOR pathway.
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