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[Ischemic heart disease and apoptosis]

G Takemura1, M Ohno, H Fujiwara

  • 1Second Department of Internal Medicine, Gifu University School of Medicine.

Rinsho Byori. the Japanese Journal of Clinical Pathology
|July 1, 1997
PubMed
Summary

Apoptosis is thought to cause cell death in ischemic heart disease. However, this study found no evidence of apoptosis in cardiomyocytes after myocardial infarction, suggesting oncotic necrosis is the primary cell death mechanism.

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Area of Science:

  • Cardiovascular Research
  • Cell Biology
  • Pathology

Context:

  • Apoptosis is widely believed to contribute to cardiomyocyte death following myocardial infarction.
  • Previous studies relied on DNA fragmentation (TUNEL) to infer apoptosis, overlooking morphological evidence.
  • Ischemic heart diseases, including myocardial infarction, involve complex cell death pathways.

Purpose:

  • To investigate the role of apoptosis in cardiomyocyte death after myocardial infarction.
  • To differentiate between apoptosis and other cell death mechanisms using combined ultrastructural and biochemical analysis.
  • To clarify the cell death pathways involved in ischemic heart disease.

Summary:

  • This study utilized electron microscopy combined with TUNEL (EM-TUNEL) to simultaneously assess ultrastructural changes and DNA fragmentation in cardiomyocytes post-myocardial infarction in rabbits.
  • Results showed oncotic necrosis, not apoptosis, as the predominant cell death mechanism in infarcted cardiomyocytes across various reperfusion times.
  • No ultrastructural evidence of apoptosis was found, challenging the prevailing view of apoptosis's role in acute ischemic cardiomyocyte death.

Impact:

  • Revises the understanding of cardiomyocyte death mechanisms in myocardial infarction.
  • Highlights the limitations of relying solely on DNA fragmentation assays for apoptosis detection.
  • Suggests that 'apoptotic' cardiomyocytes observed in previous studies may represent a different form of cell death, potentially oncotic necrosis.

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