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Mitochondrial and Nuclear DNA Oxidative Damage in Physiological and Pathological Aging.
DNA and Cell Biology ( IF 3.1 ) Pub Date : 2020-07-30 , DOI: 10.1089/dna.2019.5347
Marta Kowalska 1 , Thomas Piekut 1 , Michal Prendecki 1 , Agnieszka Sodel 1 , Wojciech Kozubski 2 , Jolanta Dorszewska 1
Affiliation  

Mitochondria play an important role in numerous processes, including energy generation, regulating ion homeostasis, and cell signaling. Mitochondria are also the main source of reactive oxygen species (ROS). Due to the oxidative environment within mitochondria, the macromolecules therein, for example, mtDNA, proteins, and lipids are more susceptible to sustaining damage. During aging, mitochondrial functions decline, partly as a result of an accumulation of mtDNA mutations, decreased mtDNA copy number and protein expression, and a reduction in oxidative capacity. The aim of this study was to summarize the knowledge on DNA oxidative damage in aging and age-related neurodegenerative diseases. It has been hypothesized that various ROS may play an important role not only in physiological senescence but also in the development of neurodegenerative diseases, for example, Alzheimer's disease and Parkinson's disease. Thus, mitochondria seem to be a potential target of novel treatments for neurodegenerative diseases.

中文翻译:

生理和病理性衰老中的线粒体和核DNA氧化损伤。

线粒体在许多过程中发挥重要作用,包括能量产生,调节离子稳态和细胞信号传导。线粒体也是活性氧(ROS)的主要来源。由于线粒体内的氧化环境,其中的大分子(例如mtDNA,蛋白质和脂质)更容易遭受破坏。在衰老过程中,线粒体功能下降,部分原因是mtDNA突变的积累,mtDNA拷贝数和蛋白质表达的降低以及氧化能力的降低。这项研究的目的是总结有关衰老和与年龄有关的神经退行性疾病中DNA氧化损伤的知识。据推测,各种ROS不仅在生理衰老中而且在神经退行性疾病例如阿尔茨海默氏病和帕金森氏病的发展中都可能起重要作用。因此,线粒体似乎是神经退行性疾病的新疗法的潜在目标。
更新日期:2020-08-04
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