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Related Concept Videos

Shock Waves01:16

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While deriving the Doppler formula for the observed frequency of a sound wave, it is assumed that the speed of sound in the medium is greater than the source's speed through it. When this condition is breached, a shock wave occurs.
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Gene therapy is a technique where a gene is inserted into a person’s cells to prevent or treat a serious disease. The added gene may be a healthy version of the gene that is mutated in the patient, or it could be a different gene that inactivates or compensates for the patient’s disease-causing gene. For example, in patients with severe combined immunodeficiency (SCID) due to a mutation in the gene for the enzyme adenosine deaminase, a functioning version of the gene can be...
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Related Experiment Video

Updated: Feb 4, 2026

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

Yunhe Zhang1,2,3, Tao Shen4, Bing Liu2

  • 1Graduate School of Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|September 25, 2018
PubMed
Summary

Cardiac shock wave therapy (CSWT) reduces heart cell death after acute myocardial infarction (AMI) in rats. CSWT protects against apoptosis by preserving mitochondrial function and inhibiting inflammatory pathways like JNK.

Keywords:
Acute myocardial infarctionApoptosisJNKShock wave therapy

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Area of Science:

  • Cardiovascular Research
  • Cell Biology
  • Regenerative Medicine

Background:

  • Cardiac shock wave therapy (CSWT) shows promise in improving cardiac function and remodeling post-ischemia.
  • Cardiomyocyte apoptosis is a critical determinant of heart function and prognosis following myocardial infarction.
  • The efficacy of CSWT in mitigating acute myocardial infarction (AMI)-induced cardiomyocyte apoptosis in vivo remains largely unexplored.

Purpose of the Study:

  • To investigate the protective effects of CSWT against cardiomyocyte apoptosis in a rat model of AMI.
  • To elucidate the underlying molecular mechanisms by which CSWT influences cardiomyocyte survival and inflammation.

Main Methods:

  • An AMI rat model was established using left anterior descending coronary artery ligation.
  • Rats were divided into sham, sham+CSWT, AMI, and AMI+CSWT groups.
  • Apoptosis was assessed via TUNEL assay, mitochondrial integrity via cytochrome c release, and signaling pathways via Western blot.

Main Results:

  • CSWT was successfully implemented in the AMI rat model.
  • CSWT significantly attenuated cardiomyocyte apoptosis in the infarct border zone.
  • CSWT suppressed the expression of apoptosis and inflammation markers, including inhibition of the JNK pathway.

Conclusions:

  • CSWT demonstrates a protective effect against AMI-induced cardiomyocyte apoptosis.
  • The mechanism involves preserving mitochondrial integrity by attenuating cytochrome c release.
  • CSWT inhibits the mitochondrial-dependent intrinsic apoptotic pathway and suppresses the JNK pathway, reducing inflammation and promoting cardiomyocyte survival.