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| 铁代谢异常诱发骨骼肌萎缩潜在机制及其运动干预研究 |
| Progress in the study of potential mechanisms of skeletal muscle atrophy induced by abnormal iron metabolism and its exercise intervention |
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| DOI：10.3969/j.issn.1006-7108.2025.12.020 |
| 中文关键词: 铁 骨骼肌萎缩 运动 |
| 英文关键词:iron skeletal muscle atrophy exercise |
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| 中文摘要: |
| 铁是人体必须的微量元素，约70%存在于血红蛋白和肌红蛋白中，参与肌细胞多种生理过程，缺铁和铁超载都会引起骨骼肌萎缩。缺铁导致肌细胞生长停滞和死亡，缺铁后肌细胞中线粒体数量减少和功能下降导致肌细胞能量代谢紊乱。铁超载引起肌细胞活性活性氧（Reactive oxygen species,ROS）产生和脂质过氧化物反应，引起自由基产生增加损害脂质、蛋白质和核酸，导致肌细胞损伤和死亡。铁超载激活肌肉环指蛋白1(Muscle Ring Finger 1,MuRF1)促进骨骼肌退化，抑制蛋白激酶B(proteinkinaseB,Akt)/叉头框蛋白O1(forkhead box protein O1,FOXO1)信号通路，导致肌肉质量下降。运动后铁蛋白受体表达增加，肌肉对铁的摄取增加，并降低肌肉中铁蛋白含量，促进肠道对铁吸收和利用。因此，深入探究铁代谢异常与骨骼肌萎缩及其运动之间的关系，对于预防和治疗铁代谢异常诱发骨骼肌萎缩具有重要意义。 |
| 英文摘要: |
| Iron is an essential trace element, about 70% of which is found in hemoglobin and myoglobin, and is involved in a variety of physiological processes in myocytes. Iron deficiency and iron overload can cause skeletal muscle atrophy.Iron deficiency leads to stagnation of growth and death of myocytes, and the decrease in the number and function of mitochondria in myocytes after iron deficiency leads to disorders of energy metabolism in myocytes.Iron overload induces reactive oxygen species (ROS) and lipid peroxidation reactions in myocytes, causing free radicals to be generated that damage lipids, proteins, and nucleic acids, leading to myocyte damage and death.Iron overload activates Muscle Ring Finger 1 (MuRF1) to promote skeletal muscle degeneration and inhibits protein kinase B (Akt)/forkhead box protein O1 (FOXO1) signaling pathway, resulting in muscle mass loss.Increased ferritin receptor expression after exercise increases muscle iron uptake and decreases ferritin levels in muscle, promoting intestinal iron absorption and utilization.Therefore, an in-depth investigation of the relationship between abnormal iron metabolism and skeletal muscle atrophy and its exercise is important for the prevention and treatment of abnormal iron metabolism-induced skeletal muscle atrophy. |
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