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

Ken Shinmura

研究成果: Article査読

抄録

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.

本文言語English
ページ(範囲)18-25
ページ数8
ジャーナルTrends in Cardiovascular Medicine
23
1
出版ステータスPublished - 2013 1

ASJC Scopus subject areas

  • 循環器および心血管医学

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