Myocyte hypertrophy and apoptosis: a balancing act

Cardiovasc Res. 2004 Aug 15;63(3):487-99. doi: 10.1016/j.cardiores.2004.02.013.

Abstract

In response to a variety of extrinsic and intrinsic stimuli that impose increased biomechanical stress the heart responds by enlarging the individual myofibers. Even though myocardial hypertrophy can normalize wall tension, it instigates an unfavorable outcome and threatens affected patients with sudden death or progression to overt heart failure, suggesting that in most instances hypertrophy is a maladaptive process. Increasing evidence suggests that several of the signaling cascades controlling myocyte growth in the adult heart also function to enhance survival of the myocyte population in response to pleiotropic death stimuli. In this review, we summarize recent insights into hypertrophic signaling pathways and their ability to control the balance between myocyte life and death. As modulation of myocardial growth by antagonizing intracellular signaling pathways is increasingly recognized as a potentially auspicious approach to prevent and treat heart failure, the design of such therapies should respect the dichotomous action of pathways that dictate a balance between myocyte hypertrophy, survival and death.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis
  • Calcium Signaling / physiology
  • Cardiomyopathy, Dilated / metabolism
  • Cardiomyopathy, Dilated / pathology*
  • Cell Death
  • Cell Size
  • Humans
  • Myocytes, Cardiac / metabolism
  • Myocytes, Cardiac / pathology*
  • NF-kappa B / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Protein Serine-Threonine Kinases / metabolism
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-akt
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • NF-kappa B
  • Proto-Oncogene Proteins
  • Tumor Necrosis Factor-alpha
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt