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Alterations in apoptosis regulatory factors during hypertrophy and heart failure

Peter M Kang1, Patrick Yue, Zhilin Liu

  • 1Cardiovascular Division, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Ave., SL-423C, Boston, MA 02215, USA. pkang@bidmc.harvard.edu

American Journal of Physiology. Heart and Circulatory Physiology
|March 6, 2004
PubMed

Insights

Physiological cardiac hypertrophy from exercise promotes survival, while pathological hypertrophy from a high-salt diet increases heart failure risk due to heightened cardiomyocyte apoptosis. This study reveals distinct molecular pathways governing these outcomes.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Pathology

Background:

  • Cardiac hypertrophy can be physiological (e.g., exercise) or pathological (e.g., high-salt diet).
  • Pathological cardiac hypertrophy often progresses to heart failure, while physiological hypertrophy typically does not.
  • Understanding the molecular differences is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the differential effects of physiological and pathological cardiac hypertrophy on cardiomyocyte apoptosis.
  • To identify the molecular mechanisms underlying the distinct outcomes of these hypertrophy types.
  • To explore the role of apoptosis in the progression of pathological cardiac hypertrophy to heart failure.

Main Methods:

  • Induction of physiological hypertrophy via daily exercise regimen in Dahl salt-sensitive rats.
  • Induction of pathological hypertrophy via high-salt diet in Dahl salt-sensitive rats.
  • Analysis of cardiomyocyte apoptosis using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay.
  • Examination of apoptosis-related molecular changes, including Bcl-2 family members and caspases, in primary heart cell cultures.

Main Results:

  • Physiological hypertrophy was associated with molecular changes favoring cardiomyocyte survival.
  • Pathological hypertrophy led to increased cardiomyocyte sensitivity to apoptosis.
  • Pathological hypertrophy exhibited diffuse proapoptotic molecular changes, including alterations in Fas, Bcl-2 family proteins, and caspases.
  • Rats on a high-salt diet progressed to heart failure with increased TUNEL-positive cardiomyocytes.

Conclusions:

  • Cardiac hypertrophy induced by pathological stimuli increases cardiomyocyte susceptibility to apoptosis.
  • Proapoptotic molecular changes in pathological cardiac hypertrophy may contribute to the development of heart failure.
  • Distinct molecular pathways govern survival and apoptosis in physiological versus pathological cardiac hypertrophy.

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