Nutrient availability links mitochondria, apoptosis, and obesity

被引：32
作者：
Pintus, Francesca [1 ,2 ]
Floris, Giovanni [2 ]
Rufini, Alessandro [1 ]
机构：
[1] Univ Leicester, Toxicol Unit, MRC, Leicester LE1 1QH, Leics, England
[2] Univ Cagliari, Dipartimento Sci Vita & Ambiente, I-09042 Monserrato, Italy
来源：
AGING-US | 2012年 / 4卷 / 11期
基金：
英国医学研究理事会;
关键词：
nutrients; obesity; caloric restriction; apoptosis; mitochondria; aging; CANCER-CELL METABOLISM; HUMAN SKELETAL-MUSCLE; OXIDATIVE-PHOSPHORYLATION; DIETARY RESTRICTION; INSULIN-RESISTANCE; AGING PHENOTYPES; CYTOCHROME-C; LIFE-SPAN; 2A GENE; DEATH;
D O I：
10.18632/aging.100505
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Mitochondria are the dominant source of the cellular energy requirements through oxidative phosphorylation, but they are also central players in apoptosis. Nutrient availability may have been the main evolutionary driving force behind these opposite mitochondrial functions: production of energy to sustain life and release of apoptotic proteins to trigger cell death. Here, we explore the link between nutrients, mitochondria and apoptosis with known and potential implications for age-related decline and metabolic syndromes.
引用
收藏
页码：734 / 741
页数：8
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