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Updated: Jun 30, 2026
Shock Wave Application to Cell Cultures
Published on: April 8, 2014
Extracorporeal cardiac shock wave therapy modulates post-infarction neovascularization via CAC-mediated
1Cardiovascular Clinical Medicine Center, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
Insights
Cardiac shock wave therapy (CSWT) activates circulating angiogenic cells (CACs) by modulating the S100A4/CSF2/FOXO1 network, offering a new therapeutic approach for ischemic heart disease (IHD) and acute myocardial infarction (AMI).
Area of Science:
- Cardiovascular Research
- Regenerative Medicine
- Molecular Biology
Background:
- Ischemic heart disease (IHD) is a leading global cause of mortality with limited long-term benefits from revascularization.
- Cardiac shock wave therapy (CSWT) shows potential in promoting neovascularization and reducing myocardial injury in IHD.
- The precise mechanisms of CSWT, particularly involving circulating angiogenic cells (CACs) and their protein interactions, require elucidation.
Purpose of the Study:
- To investigate the underlying mechanisms of CSWT in enhancing angiogenesis and mitigating structural damage post-acute myocardial infarction (AMI).
- To identify key regulatory proteins involved in CSWT-mediated angiogenesis and therapeutic effects.
Main Methods:
- Combined in vivo and in vitro experimental models.
- Olink proteomics for high-throughput protein screening.
- Quantitative PCR (qPCR) for gene expression analysis.
- Assessment of cell migration, tube formation, infarct size, and vascular markers.
Main Results:
- CSWT enhanced migration and tube formation of CACs and increased pro-angiogenic factors (VEGF, HGF) in vitro.
- In vivo, CSWT reduced infarct size, increased CACs (CD34/CD133) and vascular markers (CD31/α-SMA) post-AMI.
- Olink proteomics identified S100A4, CSF2, and FOXO1 as key regulatory proteins, with expression levels confirmed by qPCR.
Conclusions:
- CSWT activates CACs in the context of AMI by modulating the S100A4/CSF2/FOXO1 protein network.
- These findings provide a mechanistic basis for CSWT as a potential adjuvant therapy for IHD.
Abstract:
Ischemic heart disease (IHD) remains the leading cause of mortality worldwide, and the long-term benefits conferred by revascularization are limited. Cardiac shock wave therapy (CSWT) can promote neovascularization and attenuate myocardial injury, and has been applied in the treatment of IHD; its mechanism may involve Circulating Angiogenic cells (CACs) and their key proteins. This study aimed to explore the potential mechanism by which CSWT exerts effects on angiogenesis and attenuates structural damage following Acute Myocardial Infarction (AMI). Using in vivo and in vitro experiments combined with Olink proteomics, three core regulatory proteins involved in angiogenesis, namely S100A4, CSF2, and FOXO1, were screened. In vitro, optimized CSWT enhanced the migration and tube formation of rat bone marrow-derived CACs, as well as the expression of pro-angiogenic factors such as VEGF and HGF. In vivo, CSWT after AMI reduced infarct size, elevated the levels of CACs (CD34/CD133) and vascular markers (CD31/α-SMA), and modulated 18 differentially expressed proteins. Key regulatory factors S100A4, CSF2, and FOXO1 were identified by Olink proteomics. The expression levels of these proteins were verified by dual qPCR experiments in vitro and in vivo. The results reveal that CSWT modulates the S100A4/CSF2/FOXO1 network and activates CACs in AMI, suggesting a mechanistic basis for further translational evaluation of CSWT as a potential adjuvant therapy for IHD.