Choi Min Hee, Ow Jin Rong, Yang Nai-Di, Taneja Reshma
Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597; NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore 117597.
Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597.
Oxid Med Cell Longev. 2016;2016:6842568. doi: 10.1155/2016/6842568. Epub 2015 Dec 22.
Oxidative stress is a loss of balance between the production of reactive oxygen species during cellular metabolism and the mechanisms that clear these species to maintain cellular redox homeostasis. Increased oxidative stress has been associated with muscular dystrophy, and many studies have proposed mechanisms that bridge these two pathological conditions at the molecular level. In this review, the evidence indicating a causal role of oxidative stress in the pathogenesis of various muscular dystrophies is revisited. In particular, the mediation of cellular redox status in dystrophic muscle by NF-κB pathway, autophagy, telomere shortening, and epigenetic regulation are discussed. Lastly, the current stance of targeting these pathways using antioxidant therapies in preclinical and clinical trials is examined.
氧化应激是细胞代谢过程中活性氧产生与清除这些物质以维持细胞氧化还原稳态的机制之间的平衡失调。氧化应激增加与肌肉萎缩症有关,许多研究提出了在分子水平上连接这两种病理状况的机制。在本综述中,重新审视了表明氧化应激在各种肌肉萎缩症发病机制中起因果作用的证据。特别讨论了核因子κB通路、自噬、端粒缩短和表观遗传调控在营养不良性肌肉中对细胞氧化还原状态的介导作用。最后,研究了在临床前和临床试验中使用抗氧化疗法靶向这些通路的当前立场。