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Cardiovascular Research 2005 68(2):186-196; doi:10.1016/j.cardiores.2005.06.025
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Copyright © 2005, European Society of Cardiology

Protein turnover in cardiac cell growth and survival

Nadia Hedhli, Michel Pelat and Christophe Depre*

Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, University of Medicine and Dentistry New Jersey, New Jersey Medical School, 185 South Orange Avenue, MSB G-609, Newark, NJ 07103, United States.

* Corresponding author. Email address: deprech{at}umdnj.edu

Protein turnover represents the balance between protein synthesis and degradation. It can be controlled quantitatively, for instance by an activation of protein synthesis during cardiac hypertrophy or by activating protein degradation during ventricular unloading. It can also be regulated qualitatively by changing the steady state concentration of specific proteins and enzymes. The recent literature points to an emerging role for the mammalian target of rapamycin (mTOR) and for the ubiquitin–proteasome system (UPS) in this process, and both pathways interact in the regulation of cell growth and survival. We highlight the critical role played by such interaction in different cellular functions, including insulin signaling, stress response to hypoxia, adaptation to variations in workload, regulation of protein phosphatase activity, apoptosis and post-ischemic recovery. A deregulation of these pathways participates in the mechanisms of cardiac ischemia, hypertrophy and failure, and controlling their activity represents an opportunity for novel therapeutic avenues.

Time for primary review 24 days


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