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Related Experiment Videos

Apoptosis and cardiomyopathy.

J Narula1, F D Kolodgie, R Virmani

  • 1MCP-Hahnemann University School of Medicine, Philadelphia, Pennsylvania, USA.

Current Opinion in Cardiology
|August 22, 2000
PubMed
Summary
This summary is machine-generated.

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Apoptosis, a programmed cell death, occurs in adult heart muscle cells in heart failure. This cell death contributes to systolic dysfunction due to mitochondrial and protein loss.

Area of Science:

  • Cardiology
  • Cell Biology
  • Pathology

Background:

  • Apoptosis is genetically programmed cell death, distinct from necrosis.
  • Terminally differentiated adult heart muscle cells were previously thought resistant to apoptosis.
  • Heart failure is associated with ventricular dilatation and neurohormonal activation.

Purpose of the Study:

  • To investigate the presence and mechanism of apoptosis in adult heart muscle cells in heart failure.
  • To explore the relationship between apoptosis and systolic dysfunction in heart failure.

Main Methods:

  • Histochemical analysis of endomyocardial biopsies from patients with dilated and ischemic cardiomyopathy.
  • Examination of explanted hearts from patients with end-stage heart failure.

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Main Results:

  • Histochemical evidence confirmed apoptosis in adult heart muscle cells from failing hearts.
  • Proposed mechanism involves upregulation of transcription factors, myocyte hypertrophy, and attempted cell cycle entry.
  • Failed cell division leads to apoptosis, initiated by cytochrome c release and caspase activation.
  • Caspase activation results in cytoplasmic protein fragmentation, but nuclear fragmentation is rare.

Conclusions:

  • Apoptosis occurs in adult heart muscle cells during heart failure.
  • The release of cytochrome c and loss of cytoplasmic proteins are hypothesized to cause systolic dysfunction.