Regulation of skeletal muscle mitochondrial function: genes to proteins.
Regulation of skeletal muscle mitochondrial function: genes to proteins.
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DOI：
10.1111/j.1748-1716.2010.02124.x
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发表时间：
2010-08
期刊：
影响因子：
--
通讯作者：
Sreekumaran Nair K
中科院分区：
文献类型：
--
作者：
Lanza IR;Sreekumaran Nair K
衰老对线粒体功能的影响以及线粒体对衰老的决定性作用仍然是激烈争论的话题。许多研究报道骨骼肌线粒体含量和功能随着与胰岛素抵抗相关的衰老和代谢疾病而降低。然而，越来越多的文献表明，与实际年龄本身相比，身体活动不足可能是线粒体功能的一个更重要的决定因素。关于年龄相关的线粒体功能下降的报道已经产生了大量的文献，致力于了解潜在的机制。这些机制包括线粒体DNA丰度降低，mRNA水平降低，以及线粒体蛋白质合成和表达减少，最终导致整个细胞器功能下降。有效的治疗，以防止逆转，或延迟上述线粒体变化的发生，无论其不可避免性或确切的根本原因，需要密切了解的过程，调节线粒体生物发生，这需要协调调节核和线粒体基因组。在此，我们回顾了目前的思想调节线粒体生物合成的转录因子和转录辅激活因子和激素的作用和运动在启动这一进程。我们回顾了运动如何有助于在整个生命周期中保护线粒体的内容和功能，以及身体活动如何成为许多年龄相关变化的主要决定因素。我们还回顾了一些线粒体随年龄增长而变化的证据，这些变化与运动或体力活动无关，似乎是老年不可避免的后果。
The impact of aging on mitochondrial function and the deterministic role of mitochondria on scenescence continue to be topics of vigorous debate. Many studies report that skeletal muscle mitochondrial content and function are reduced with aging and metabolic diseases associated with insulin resistance. However, an accumulating body of literature suggests that physical inactivity typical of aging may be a more important determinant of mitochondrial function than chronological age, per se. Reports of age-related declines in mitochondrial function have spawned a vast body of literature devoted to understanding the underlying mechanisms. These mechanisms include decreased abundance of mtDNA, reduced mRNA levels, as well as decreased synthesis and expression of mitochondrial proteins, ultimately resulting in decreased function of the whole organelle. Effective therapies to prevent reverse, or delay the onset of the aformentioned mitochondrial changes, regardless of their inevitability or precise underlying causes, require an intimate understanding of the processes that regulate mitochondrial biogenesis, which necessitates the coordinated regulation of nuclear and mitochondrial genomes. Herein we review the current thinking on regulation of mitochondrial biogenesis by transcription factors and transcriptional co-activators and the role of hormones and exercise in initiating this process. We review how exercise may help preserve mitochondrial content and functionality across the lifespan, and how physical inactivity is emerging as a major determinant of many age-associated changes at the level of the mitochondrion. We also review evidence that some mitochondrial changes with aging are independent of exercise or physical activity and appear to be inevitable consequences of old age.
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影响因子：
6.7
作者：
ANIANSSON, A;GRIMBY, G;ORLANDER, J
通讯作者：
ORLANDER, J
影响因子：
3.3
作者：
Chow, Lisa S.;Greenlund, Laura J.;Nair, K. Sreekumaran
通讯作者：
Nair, K. Sreekumaran
DOI：
10.1073/pnas.82.24.8384
发表时间：
1985-12-01
影响因子：
11.1
作者：
CHANCE, B;LEIGH, JS;SMITH, D
通讯作者：
SMITH, D
影响因子：
3.5
作者：
Bota, DA;Van Remmen, H;Davies, KJA
通讯作者：
Davies, KJA
DOI：
10.1111/j.1432-1033.1992.tb16984.x
发表时间：
1992-06-15
期刊：
EUROPEAN JOURNAL OF BIOCHEMISTRY
影响因子：
--
作者：
BRAND, MD;STEVERDING, D;HAFNER, RP
通讯作者：
HAFNER, RP