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Response of caspase-independent apoptotic factors to high salt diet-induced heart failure

Parco M Siu1, Soochan Bae, Natalya Bodyak

  • 1Cardiovascular Division, Beth Israel Deaconess Medical Center, 330 Brookline Ave, SL-423C, Boston, MA 02215, USA.

Journal of Molecular and Cellular Cardiology
|February 13, 2007
PubMed

Insights

Caspase-independent apoptotic factors like AIF and EndoG are altered in late-stage heart failure. These changes suggest a role for these factors in pathological cardiac remodeling.

Area of Science:

  • Cardiovascular Research
  • Cellular Biology
  • Apoptosis

Background:

  • The role of caspase-independent apoptosis in heart failure is not well understood.
  • Apoptotic factors such as apoptosis-inducing factor (AIF), endonuclease G (EndoG), and HtrA2/Omi can function independently of caspases.

Purpose of the Study:

  • To investigate the involvement of caspase-independent apoptotic factors in high salt diet-induced heart failure and exercise-induced cardiac hypertrophy.
  • To examine the expression and subcellular localization of AIF, EndoG, and HtrA2/Omi in pathological cardiac remodeling.

Main Methods:

  • High salt diet-induced heart failure model in animals.
  • Exercise training model for physiological cardiac hypertrophy.
  • Western blotting and RT-PCR to assess protein and mRNA levels.
  • Confocal microscopy for immunofluorescence and subcellular localization studies.

Main Results:

  • High salt diet induced heart failure with altered levels of AIF, EndoG, and HtrA2/Omi.
  • Cytosolic accumulation and translocation of AIF from mitochondria to cytosol and nuclei were observed in failing ventricles.
  • AIF and EndoG mRNA levels were decreased in failing hearts.
  • No significant changes in these factors were observed in exercise-trained hearts or early high salt diet models.

Conclusions:

  • Caspase-independent apoptotic events are implicated in the late remodeling stages of pathological heart failure.
  • AIF and EndoG may play a role in cardiac apoptosis during advanced heart failure.
  • These findings contribute to understanding the mechanisms of heart failure progression.

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