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Cardiovascular Research 2004 63(3):487-499; doi:10.1016/j.cardiores.2004.02.013
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Myocyte hypertrophy and apoptosis: a balancing act

Vanessa P.M van Empel and Leon J De Windt*

Hubrecht Laboratory and Interuniversity Cardiology Institute Netherlands, Royal Netherlands Academy of Arts and Sciences, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands

* Corresponding author. Tel.: +31-30-2121800; fax: +31-30-2121801. Email address: dewindt{at}niob.knaw.nl

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 controling 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.

KEYWORDS Apoptosis; Hypertrophy; Heart failure; Mitochondria

Time for primary review for 25 days


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