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

Ken Shinmura

Research output: Contribution to journalArticle

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.

Original languageEnglish
Pages (from-to)18-25
Number of pages8
JournalTrends in Cardiovascular Medicine
Volume23
Issue number1
Publication statusPublished - 2013 Jan

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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