Post-translational modification of mitochondrial proteins by caloric restriction: possible involvement in caloric restriction-induced cardioprotection.

Abstract

Increasing evidence demonstrates that members of the sirtuin family, most of which work as NAD(+)-dependent protein deacetylases, mediate the preferable effects of caloric restriction. Since mitochondria play a central role in cardiac reactive oxygen species production, targeted modification of mitochondrial proteins and subsequent improvement in mitochondrial function have the potential for controlling cardiovascular senescence and managing cardiovascular diseases such as ischemia/reperfusion. We showed that caloric restriction primes cardiac mitochondria for ischemic stress by deacetylating specific mitochondrial proteins of the electron transport chain. We speculate that deacetylation of specific mitochondrial proteins by sirtuin preserves mitochondrial function and attenuates myocardial oxidative damage during ischemia/reperfusion.

• Authors: Ken Shinmura
• Journal: Trends in cardiovascular medicine (Trends Cardiovasc Med) Vol. 23 Issue 1 Pg. 18-25 (Jan 2013) ISSN: 1873-2615 [Electronic] United States
• PMID: 23312135 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
• Copyright: Copyright © 2013 Elsevier Inc. All rights reserved.

Chemical References

• Cardiotonic Agents
• Mitochondrial Proteins
• Reactive Oxygen Species
• Sirtuins

Topics

• Animals
• Caloric Restriction
• Cardiotonic Agents
• Humans
• Mitochondria (metabolism)
• Mitochondrial Proteins (metabolism)
• Oxidative Stress
• Protein Processing, Post-Translational
• Reactive Oxygen Species (metabolism)
• Sirtuins (metabolism)