Mitochondria in response to nutrients and nutrient-sensitive pathways

被引：22

作者：

Baltzer, Claudia ^{[1
]}

Tiefenbock, Stefanie K. ^{[1
]}

Frei, Christian ^{[1
]}

机构：

[1] ETH, Dept Biol, CH-8093 Zurich, Switzerland

来源：

MITOCHONDRION | 2010年 / 10卷 / 06期

基金：

瑞士国家科学基金会;

关键词：

Mitochondria; Nutrients; TCA cycle; Oxidative phosphorylation; Microarray; NUCLEAR RESPIRATORY FACTOR-1; TRANSCRIPTION FACTOR GABP; GENE-EXPRESSION; CALORIC RESTRICTION; ENERGY-METABOLISM; SKELETAL-MUSCLE; THYROID-HORMONE; PPAR-ALPHA; TARGETED DISRUPTION; PGC-1; COACTIVATORS;

D O I：

10.1016/j.mito.2010.07.009

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Mitochondria are abundant cellular organelles and are required for the generation of energy through oxidative catabolism Equally important mitochondria also provide substrates for de novo synthesis of fatty acids and multiple amino acids Mitochondrial functions must therefore be tightly linked to cellular nutrient availability This review focuses on the current knowledge of how nutrients affect mitochondria In particular we describe how the transcriptional profile of the nucleus is altered to mediate this control and the transcription factors that are Involved In addition we summarize recent progress in our understanding of how transcription-independent mechanisms most notably through the cellular energy sensor mTOR are used to adapt mitochondrial functions in respect to cellular metabolic needs (C) 2010 Elsevier B V and Mitochondria Research Society All rights reserved

引用

页码：589 / 597

页数：9

共 129 条

[21] mTOR controls mitochondrial oxidative function through a YY1-PGC-1α transcriptional complex [J].