Mitochondrial aging and age-related dysfunction of mitochondria.

Mitochondrial aging and age-related dysfunction of mitochondria.
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DOI:
10.1155/2014/238463
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发表时间:
2014
影响因子:
--
通讯作者:
Bobryshev YV
Bobryshev YV
中科院分区:
生物学3区
文献类型:
--
作者:
Chistiakov DA;Sobenin IA;Revin VV;Orekhov AN;Bobryshev YV

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线粒体的年龄相关变化与线粒体功能下降有关。随着年龄的增长,由于突变的积累和活性氧 (ROS) 引起的氧化损伤,线粒体 DNA 的体积、完整性和功能都会下降。在老年受试者中,线粒体的特点是功能受损,例如氧化能力降低、氧化磷酸化减少、ATP 产生减少、ROS 生成显着增加以及抗氧化防御减弱。由于线粒体动力学的改变和线粒体自噬的抑制,线粒体生物发生随着年龄的增长而下降,线粒体自噬是一种消除功能障碍的线粒体的自噬过程。线粒体质量控制的年龄依赖性异常进一步削弱和损害线粒体功能。在衰老组织中,线粒体介导的细胞凋亡增强导致凋亡细胞百分比增加。然而,实施热量限制和定期体育锻炼等策略可能会延缓线粒体衰老并减弱人类与年龄相关的表型。
Age-related changes in mitochondria are associated with decline in mitochondrial function. With advanced age, mitochondrial DNA volume, integrity and functionality decrease due to accumulation of mutations and oxidative damage induced by reactive oxygen species (ROS). In aged subjects, mitochondria are characterized by impaired function such as lowered oxidative capacity, reduced oxidative phosphorylation, decreased ATP production, significant increase in ROS generation, and diminished antioxidant defense. Mitochondrial biogenesis declines with age due to alterations in mitochondrial dynamics and inhibition of mitophagy, an autophagy process that removes dysfunctional mitochondria. Age-dependent abnormalities in mitochondrial quality control further weaken and impair mitochondrial function. In aged tissues, enhanced mitochondria-mediated apoptosis contributes to an increase in the percentage of apoptotic cells. However, implementation of strategies such as caloric restriction and regular physical training may delay mitochondrial aging and attenuate the age-related phenotype in humans.
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