A review: oxidative stress in skeletal muscle and the non-coding RNAs behind it

Oxidative damage, primarily caused by reactive oxygen species (ROS), leads to the oxidation of cellular components, particularly in skeletal muscles. ROS accumulation in muscle fibers results in the oxidation of proteins, lipids, and nucleic acids, affecting the stability of muscle structure and function. Signaling pathways, including NF-κB, MAPK, Nrf2-ARE, PI3K-AKT, and p53 pathways, are intimately associated with oxidative stress. Understanding the impact of oxidative stress on skeletal muscles and the regulatory mechanisms of ncRNA on skeletal muscle oxidative stress is crucial for preventing muscle damage caused by oxidative stress. Oxidative stress mechanisms in skeletal muscles are intricate, and involve many regulatory factors and signaling pathways. NcRNAs play critical regulatory roles in these responses, but their specific functions and mechanisms require further research. Future research should explore in depth the interactions between ncRNAs and other molecules, providing new theoretical foundations and practical guidance for the prevention of muscle oxidative stress. This review summarizes current understanding of molecular mechanisms driving oxidative stress in skeletal muscle, with emphasis on regulatory networks mediated by ncRNAs. Future investigations should focus on multi-omics integration of ncRNA crosstalk with redox signaling pathways, potentially informing preventive strategies against muscle dysfunction in metabolic and aging-related conditions.