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神经退行性疾病中的氧化应激:损害骨骼肌健康的关键驱动因素。

Oxidative Stress in Neurodegenerative Disorders: A Key Driver in Impairing Skeletal Muscle Health.

作者信息

Castelli Serena, Carinci Emily, Baldelli Sara

机构信息

Department for the Promotion of Human Science and Quality of Life, San Raffaele Open University, Via di Val Cannuta, 247, 00166 Rome, Italy.

IRCCS San Raffaele Roma, 00166 Rome, Italy.

出版信息

Int J Mol Sci. 2025 Jun 16;26(12):5782. doi: 10.3390/ijms26125782.

Abstract

The fine regulation of antioxidant systems and intracellular production of reactive oxygen species (ROS) is responsible for cellular redox balance. The main organelles responsible for ROS production are mitochondria, and they complete this process through the electron transport chain. These potentially harmful molecules are buffered by enzymatic and non-enzymatic antioxidant systems. Oxidative stress is determined by an imbalance between the production and clearance of ROS in favor of the accumulation of these detrimental species, which generate cellular damage by interacting with macromolecules. In neurodegenerative diseases, oxidative stress has been demonstrated to be a crucial component, both causal and consequential to the disease itself. On the other hand, neurodegeneration disrupts neuromuscular junctions, leading to reduced muscle use and subsequent atrophy. Additionally, systemic inflammation and metabolic dysfunction associated with neurodegenerative diseases exacerbate muscle degeneration. Thus, sarcopenia and atrophy are common consequences of neurodegeneration and play a significant role in these disorders. Regarding this, ROS have been defined as promoting sarcopenia, stimulating the expression of genes typical of this condition. Overall, this review aims to contribute to filling the gap in the literature regarding the consequences at the muscular level of the relationship between oxidative stress and neurodegenerative diseases.

摘要

抗氧化系统的精细调节以及细胞内活性氧(ROS)的产生负责维持细胞的氧化还原平衡。负责产生ROS的主要细胞器是线粒体,它们通过电子传递链完成这一过程。这些潜在有害分子由酶促和非酶促抗氧化系统进行缓冲。氧化应激取决于ROS产生与清除之间的失衡,导致这些有害物质积累,它们通过与大分子相互作用造成细胞损伤。在神经退行性疾病中,氧化应激已被证明是一个关键因素,既是疾病的起因,也是疾病导致的结果。另一方面,神经退行性变会破坏神经肌肉接头,导致肌肉使用减少及随后的萎缩。此外,与神经退行性疾病相关的全身炎症和代谢功能障碍会加剧肌肉退化。因此,肌肉减少症和萎缩是神经退行性变的常见后果,并在这些疾病中起重要作用。关于这一点,ROS已被定义为促进肌肉减少症,刺激这种状况典型基因的表达。总体而言,本综述旨在填补文献中关于氧化应激与神经退行性疾病之间关系在肌肉层面后果的空白。

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