Shock wave therapy of ischemic heart disease in the light of general pathology

Jargin, Sergei V.

doi:10.1016/j.ijcard.2008.12.198

Cited by 11 publications

(11 citation statements)

References 19 publications

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“…However, there also has some conflicting viewpoint for CSWT, indicating that CSWT can cause irreversible myocardial damage and may cause an injury-and-repair process, which is expected to result in fibrosis and functional loss of the myocardium [39,40]. Given the lack of safety studies, an Italy study evaluates the safety of CSWT on the adult heart and its effects on cardiac tissue function and morphology.…”

Section: Discussionmentioning

confidence: 99%

Cardiac Shock Wave Therapy Attenuates H9c2 Myoblast Apoptosis by Activating the AKT Signal Pathway

Shen

Liu

et al. 2014

Cell Physiol Biochem

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Background: Previous studies have demonstrated that Cardiac Shock Wave Therapy (CSWT) improves myocardial perfusion and cardiac function in a porcine model of chronic myocardial ischemia and also ameliorates myocardial ischemia in patients with severe coronary artery disease (CAD). Apoptosis plays a key role in ischemic myocardial pathogenesis. However, it remains unclear whether CSWT is beneficial for ischemia/hypoxia (I/H)-induced myocardial cell apoptosis and by which mechanism CSWT could improve heart function. We put forward the hypothesis that CSWT might protect heart function during ischemia/hypoxia by decreasing apoptosis. Methods: We generated ischemia/hypoxia (I/H)-induced apoptosis in the H9c2 myoblast cell line to examine the CSWT function and possible mechanisms. H9c2 cells were treated under hypoxic serum-starved conditions for 24 h and then treated with or without CSWT (500 shots, 0.06, 0.09, 0.12mJ/mm²). The apoptotic cell rate was determined by flow cytometry assay, cell viability was examined by the MTT assay, nuclear fragmentation was detected by Hoechst 33342 staining, and the mitochondrial-mediated intrinsic pathway of apoptosis was assessed by the expression of Bax and Bcl-2 protein and Caspase3 activation. Results: First, apoptosis could be induced by ischemia/hypoxia in H9c2 cells. Second, CSWT attenuates the cell death and decreases the H9c2 cell apoptosis rate induced by ischemia and hypoxia. Third, CSWT suppresses the expression of apoptosis molecules that regulate the intrinsic pathway of apoptosis in H9c2 cells. Fourth, CSWT increases the phosphorylation of AKT, which indicates the activation of the PI3K-AKT pathway. Conclusions: These results indicate that CSWT exerts a protective effect against I/H-induced cell death, potentially by preventing the activation of components of the mitochondrial-dependent intrinsic apoptotic pathway. We also demonstrate that the PI3K-Akt pathway may be involved in the CSWT effects on apoptosis.

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Section: Discussionmentioning

confidence: 99%

Cardiac Shock Wave Therapy Attenuates H9c2 Myoblast Apoptosis by Activating the AKT Signal Pathway

Shen

Liu

et al. 2014

Cell Physiol Biochem

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“…As a new and non-invasive treatment strategy for ischemic heart disease, the safety of CSWT is still controversial. Sergei [39] considers shock wave therapy to be an unselective damaging factor that would injure cell membranes and the cytoskeleton. To assess the safety of CSWT on cardiac tissue function and structure, Di et al [40] deliver low-energy shock waves (100 shots, 0.25 mJ/mm 2 ) to normal Fisher 344 rats.…”

Section: Mechanisms Of the Suppression Effects Of Cswt On Cardiomyocymentioning

confidence: 99%

Cardiac Shock Wave Therapy Attenuates Cardiomyocyte Apoptosis after Acute Myocardial Infarction in Rats

Zhang

Shen

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Researches have showed that cardiac shock wave therapy (CSWT) could improve left ventricular function and attenuate LV remodeling of the ischemic heart. Apoptosis plays an important role in myocardial infarction and determines heart function and prognosis. However, it is still not clear whether CSWT is sufficient to attenuate acute myocardial infarction (AMI) induced cardiomyocyte apoptosis in vivo. In this study, we used a rat model to examine whether CSWT could attenuate cardiomyocyte apoptosis after AMI and to explore potential mechanisms. Methods: We generated an AMI rat model to investigate the function and possible regulatory mechanisms of CSWT. All rats were randomly divided into four groups: the sham-operated only group, sham-operated with SW treatment group, AMI only group, and AMI treated with SW treatment group.The rats were treated with a left anterior descending coronary artery ligation for 12h and then treated with or without CSWT (800 shots at 0.1 mJ/ mm²). Cytochrome c release was measured to analyze mitochondrial function and integrity. The apoptotic cell rate was determined by TUNEL assay. Western blot was used to analyze the cell apoptosis-, inflammation-, and survival-related signaling pathways. Results: First, the methodology of CSWT in the rat model of AMI was established. Second, CSWT attenuated the cardiomyocyte apoptosis rate in the infarct border zone. Third, CSWT suppressed the expression of apoptosis and inflammation molecules after AMI. Fourth, CSWT inhibited activation of the JNK pathway, which indicated inhibition of the cell inflammatory pathways and promotion of cardiomyocyte survival after AMI. Conclusion: These results indicate that CSWT exerts a protective effect against AMI-induced cardiomyocyte apoptosis, potentially by attenuating cytochrome c release from the mitochondria and inhibiting of the mitochondrial-dependent intrinsic apoptotic pathway. We also demonstrate that CSWT suppresses the JNK pathway and cardiomyocyte inflammation, which may also decrease cardiomyocyte apoptosis in vivo.

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“…Dear Professor Holfeld, Many thanks for your valuable comment on the paper [1]. All statements in your letter are obviously true and, at the same time, seem to be not contradictory to what I have written.…”

mentioning

confidence: 67%

“…Sergei V. Jargin reports in his Letter to the Editor entitled Shock wave therapy of ischemic heart disease in the light of general pathology on a device on the basis of a modified lithotripter that is currently used in Russia for the treatment of ischemic heart disease [1]. He describes shock waves as an unselective damaging factor that injures cell membranes, cytoskeleton and small vessels.…”

mentioning

confidence: 99%

“…A net benefit from shock wave therapy (SWT) of ischemic heart disease (IHD) is not immediately understandable from the viewpoint of general pathology: for example, activation of growth factors can contribute to atherogenesis and fibrosis. Further details and references are in the letter [1]. Moreover, it is generally an accepted knowledge in pathology that a physical impact, if powerful enough, can damage cells (which can be more significant if they are incapable of mitosis such as myocardial cells and pre-damaged by ischemia) and contribute to interstitial fibrosis or scarring.…”

mentioning

confidence: 99%

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Reply to Sergej V. Jargin: Shock wave therapy of ischemic heart disease in the light of general pathology

Holfeld

Zimpfer

Schaden

et al. 2010

International Journal of Cardiology

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Shock wave therapy of ischemic heart disease in the light of general pathology

Cited by 11 publications

References 19 publications

Cardiac Shock Wave Therapy Attenuates H9c2 Myoblast Apoptosis by Activating the AKT Signal Pathway

Cardiac Shock Wave Therapy Attenuates H9c2 Myoblast Apoptosis by Activating the AKT Signal Pathway

Cardiac Shock Wave Therapy Attenuates Cardiomyocyte Apoptosis after Acute Myocardial Infarction in Rats

Reply to Sergej V. Jargin: Shock wave therapy of ischemic heart disease in the light of general pathology

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