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Apoptosis in the failing human heart
1Department of Medicine, New York Medical College, Valhalla 10595, USA.
The New England Journal of Medicine
|April 17, 1997
Summary
Programmed cell death (apoptosis) significantly increases in heart failure patients, even with higher BCL2 expression. This myocyte loss may worsen cardiac dysfunction.
Area of Science:
- Cardiology
- Cell Biology
- Molecular Medicine
Background:
- Myocyte loss is a key factor in cardiac failure development.
- The role of programmed cell death (apoptosis) in end-stage heart failure was previously unknown.
Purpose of the Study:
- To investigate the extent of myocyte apoptosis in patients with severe congestive heart failure.
Main Methods:
- Analyzed myocardial samples from heart transplant recipients, post-myocardial infarction patients, and healthy controls.
- Assessed apoptosis using histochemical and biochemical methods, including confocal microscopy.
- Quantified the expression of apoptosis-regulating genes BCL2 and BAX.
Main Results:
- Heart failure hearts showed a 232-fold increase in myocyte apoptosis, confirmed by DNA laddering and morphological changes.
- BCL2 expression, a cell survival gene, was 1.8 times higher in failing hearts, while BAX expression remained unchanged.
- Western blotting confirmed the increased BCL2 levels in cardiac tissue from heart failure patients.
Conclusions:
- Programmed myocyte death occurs in decompensated human hearts.
- Despite increased BCL2 expression, myocyte apoptosis persists and may contribute to worsening cardiac dysfunction.