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Striking a balance: autophagy, apoptosis, and necrosis in a normal and failing heart

Wajihah Mughal1, Rimpy Dhingra, Lorrie A Kirshenbaum

  • 1The Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Department of Physiology, University of Manitoba, Winnipeg, Canada.

Current Hypertension Reports
|September 25, 2012
PubMed

Insights

Heart failure is a major global health issue. Defects in cellular processes like autophagy, apoptosis, and necrosis, involving specific molecular pathways, are key causes of heart failure in ischemic heart disease.

Area of Science:

  • Cardiovascular Research
  • Cellular Biology
  • Molecular Mechanisms

Background:

  • Heart failure remains a significant cause of global morbidity and mortality despite advances in cardiovascular research.
  • Ischemic heart disease contributes to heart failure through defects in cellular processes governing cell death and survival.

Purpose of the Study:

  • To review recent advances in molecular signaling factors that regulate cardiac cell fate.
  • To understand the mechanisms underlying heart failure in ischemic heart disease.

Main Methods:

  • Literature review of recent advances in molecular signaling.
  • Analysis of cellular and molecular mechanisms of cardiac cell death pathways.

Main Results:

  • Defects in autophagy, apoptosis, and necrosis are identified as prevailing causes of heart failure.
  • Programmed cell death involves intrinsic mitochondrial and extrinsic death receptor pathways, including Bcl-2 family members and TNFα signaling.

Conclusions:

  • Understanding molecular signaling in cardiac cell fate is crucial for addressing heart failure.
  • Targeting these pathways may offer therapeutic strategies for heart failure patients.

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