铁死亡在肌肉减少症发病机制中的研究进展

Research Progress of Ferroptosis in the Pathogenesis of Sarcopenia

肌肉减少症(肌少症)是一种随年龄增长而导致骨骼肌质量和力量逐渐下降的疾病,给老年人的生活质量和健康产生严重负面影响。最近,铁死亡作为一种新兴的细胞死亡机制,其与肌少症的关系受到了广泛研究。铁死亡是一种以铁元素及脂质过氧化为核心的细胞死亡方式,与肌少症的发病机制密切关联。已有研究认为铁代谢、脂质过氧化、氨基酸代谢失衡等途径在肌少症的发生中起着重要作用。特别是铁超载和活性氧的积累,以及System Xc-/GSH/GPX4轴和NADPH/FSP1/CoQ10通路之间相互作用,对于维持细胞内氧化还原平衡和防止脂质过氧化中发挥关键作用。此外,肌肉衰减型肥胖、虚弱状态与肌少症的相互关联,以及慢性疾病对肌少症的影响也不容忽视。因此文章就铁死亡在肌少症中的作用机制进行综述,未来的研究需要进一步探索铁死亡的关键调控环节,以便为肌少症发现新的治疗靶点和开发有效的干预措施提供理论基础和实践参考。

Sarcopenia,an age-related condition characterized by the progressive decline in skeletal muscle quality and strength,significantly impacts the health and quality of life of older individuals.Recently,the emergence of ferroptosis,a novel form of cell death,has garnered widespread attention.Ferroptosis is a form of programmed cell death that relies on iron and lipid peroxidation processes,closely associated with the development of sarcopenia.Disruptions in iron metabolism,lipid peroxidation,amino acid imbalances,and other pathways are identified as significant contributors to sarcopenia onset.Notably,the roles of iron overload,ROS accumulation,and the modulation of the System Xc-/GSH/GPX4 axis and NADPH/FSP1/CoQ10 pathways are crucial in maintaining cellular redox balance and preventing lipid peroxidation.Additionally,the connection between muscle mass reduction,weakness,sarcopenia,and the impact of chronic illnesses on sarcopenia cannot be overlooked.This paper reviews the mechanism of ferroptosis in sarcopenia,emphasizing the need for further investigations to identify key regulatory pathways of ferroptosis for the discovery of new therapeutic targets and effective intervention strategies.