Mitochondrial SIRT3: A new potential therapeutic target for metabolic syndrome

Jun Yoshino; Shin ichiro Imai

doi:10.1016/j.molcel.2011.10.005

Mitochondrial SIRT3: A new potential therapeutic target for metabolic syndrome

Jun Yoshino, Shin ichiro Imai

Research output: Contribution to journal › Short survey › peer-review

24 Scopus citations

Abstract

In this issue of Molecular Cell, Hirschey et al. demonstrate that loss of the NAD⁺-dependent deacetylase SIRT3 and resultant mitochondrial protein hyperacetylation play a critical role in the pathogenesis of metabolic syndrome, providing new insights into the therapeutic potential of SIRT3.

Original language	English
Pages (from-to)	170-171
Number of pages	2
Journal	Molecular cell
Volume	44
Issue number	2
DOIs	https://doi.org/10.1016/j.molcel.2011.10.005
State	Published - Oct 21 2011

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title = "Mitochondrial SIRT3: A new potential therapeutic target for metabolic syndrome",

abstract = "In this issue of Molecular Cell, Hirschey et al. demonstrate that loss of the NAD+-dependent deacetylase SIRT3 and resultant mitochondrial protein hyperacetylation play a critical role in the pathogenesis of metabolic syndrome, providing new insights into the therapeutic potential of SIRT3.",

author = "Jun Yoshino and Imai, {Shin ichiro}",

year = "2011",

month = oct,

day = "21",

doi = "10.1016/j.molcel.2011.10.005",

language = "English",

volume = "44",

pages = "170--171",

journal = "Molecular cell",

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TY - JOUR

T1 - Mitochondrial SIRT3

T2 - A new potential therapeutic target for metabolic syndrome

AU - Yoshino, Jun

AU - Imai, Shin ichiro

PY - 2011/10/21

Y1 - 2011/10/21

N2 - In this issue of Molecular Cell, Hirschey et al. demonstrate that loss of the NAD+-dependent deacetylase SIRT3 and resultant mitochondrial protein hyperacetylation play a critical role in the pathogenesis of metabolic syndrome, providing new insights into the therapeutic potential of SIRT3.

AB - In this issue of Molecular Cell, Hirschey et al. demonstrate that loss of the NAD+-dependent deacetylase SIRT3 and resultant mitochondrial protein hyperacetylation play a critical role in the pathogenesis of metabolic syndrome, providing new insights into the therapeutic potential of SIRT3.

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U2 - 10.1016/j.molcel.2011.10.005

DO - 10.1016/j.molcel.2011.10.005

M3 - Short survey

C2 - 22017865

AN - SCOPUS:82455175476

SN - 1097-2765

VL - 44

SP - 170

EP - 171

JO - Molecular cell

JF - Molecular cell

IS - 2

ER -

Mitochondrial SIRT3: A new potential therapeutic target for metabolic syndrome

Abstract

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