衰老过程中因肌肉减少症而衰弱的骨骼肌线粒体的超微结构

IF 0.6 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
V. B. Weiss, I. M. Vangeli, Ch. M. Eldarov, L. E. Bakeeva
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引用次数: 0

摘要

摘要 骨骼肌衰老过程中出现的肌肉质量逐渐减少和线粒体功能减弱的过程仍然鲜为人知,尤其是线粒体超微结构与骨骼肌萎缩过程之间的因果关系。我们对快速衰老的哺乳动物物种(Wistar 大鼠、OXYS、小鼠)和长寿物种的代表:裸鼹鼠(Heterocephalus glaber)和人类进行了骨骼肌衰老过程中线粒体内部结构组织特征的超微结构研究。结果显示,24 个月大的 OXYS 大鼠骨骼肌线粒体内部组织结构发生了之前未知的、与年龄相关的变化:每个线粒体中都出现了星状结构形式的嵴排列改变的局部区域,还出现了极大的结构形成,这显然是线粒体破坏过程的结果,还出现了大小和内部超微结构异常的线粒体。研究表明,10 个月大的小鼠和 11 岁大的裸鼹鼠的结构变化是多向的。如果说小鼠正常超微结构的紊乱不仅影响线粒体,还影响肌纤维和肌浆网,那么在鼹鼠身上不仅没有观察到病理变化,相反,线粒体发达的结构表明了这些细胞器的功能活动。首次使用活检材料对 68-81 岁和 25-28 岁人类骨骼肌线粒体的超微结构进行了比较。在老年患者中,线粒体增殖现象显现出来:这是线粒体功能障碍的一种代偿性结构反应。线粒体体积小,嵴数量少。在年轻人身上,线粒体的超微结构与骨骼肌线粒体结构组织特征的经典观点一致。研究还考虑了自噬在衰老过程中可能发挥的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Ultrastructure of Mitochondria in Skeletal Muscle Weakened by Sarcopenia during Aging

Ultrastructure of Mitochondria in Skeletal Muscle Weakened by Sarcopenia during Aging

Ultrastructure of Mitochondria in Skeletal Muscle Weakened by Sarcopenia during Aging

The processes of progressive decrease in muscle mass and weakening of mitochondrial function that occur during aging in skeletal muscles remain poorly understood as does, above all, the cause-and-effect relationship between the ultrastructure of mitochondria and atrophic processes in skeletal muscles. An ultrastructural study of the features of the internal structural organization of mitochondria during aging of skeletal muscle was carried out on representatives of rapidly aging mammalian species (Wistar rats, OXYS, mice) and representatives of long-lived species: the naked mole rat (Heterocephalus glaber) and human. Previously unknown, age-related structural changes in the internal organization of skeletal muscle mitochondria in OXYS rats at the age of 24 months are shown: the appearance in each mitochondria of local areas of altered arrangement of cristae in the form of stellate structures, as well as the presence of extremely large structural formations, apparently the result of destructive processes in mitochondria, as well as the appearance of mitochondria that are abnormal in size and internal ultrastructure. It was shown that structural changes in mice at the age of 10 months and naked mole rats at the age of 11 years were multidirectional. If disturbances in the normal ultrastructure in mice affected not only mitochondria but also muscle fibers and the sarcoplasmic reticulum, then not only no pathological changes are observed in mole rats but also, on the contrary, the powerfully developed structure of mitochondria indicates the functional activity of these organelles. For the first time, the ultrastructure of mitochondria in human skeletal muscle at the age of 68–81 and 25–28 years was compared using biopsy material. In elderly patients, the phenomenon of mitochondrial proliferation is shown: a compensatory structural response to mitochondrial dysfunction. Mitochondria are small, with a small number of cristae. In young people, the ultrastructure of mitochondria corresponded to classical ideas about the features of the structural organization of skeletal muscle mitochondria. Literary ideas about the possible role of autophagy in the development of aging processes are considered.

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来源期刊
CiteScore
1.10
自引率
0.00%
发文量
31
期刊介绍: Biochemistry (Moscow), Supplement Series B: Biomedical Chemistry   covers all major aspects of biomedical chemistry and related areas, including proteomics and molecular biology of (patho)physiological processes, biochemistry, neurochemistry, immunochemistry and clinical chemistry, bioinformatics, gene therapy, drug design and delivery, biochemical pharmacology, introduction and advertisement of new (biochemical) methods into experimental and clinical medicine. The journal also publishes review articles. All issues of the journal usually contain solicited reviews.
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