ISSN 1006-298X      CN 32-1425/R

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肾脏病与透析肾移植杂志 ›› 2013, Vol. 22 ›› Issue (2): 158-161.

• 论文 • 上一篇    下一篇

慢性肾脏病诱导骨骼肌萎缩的发病机制

  

  • 出版日期:2013-04-28 发布日期:2013-04-29

Review of muscle wasting associated with chronic kidney disease

  • Online:2013-04-28 Published:2013-04-29

摘要:

摘  要  慢性肾脏病(CKD)患者常伴有进行性、难纠正的蛋白-能量消耗(PEW),主要临床表现为骨骼肌萎缩,可增加患者并发症和死亡风险。肌萎缩的发病机制很复杂,常由多因素共同作用所致。先前研究认为食欲减退、泛素-蛋白酶体系活化及细胞内胰岛素/胰岛素样生长因子-1/PI3K/Akt信号通路受损是导致肌萎缩的主要原因。然而随着大量研究的深入进展,近年发现炎症反应、代谢性酸中毒、激素代谢紊乱和myostatin表达增加等因素在肌萎缩发生发展中也起着不可忽视的作用,但其中部分作用机制尚未完全阐明,还需深入探索,以寻找切实有效的干预靶点,改善CKD患者临床预后。

Abstract:

ABSTRACT   The patients with chronic kidney disease usually have progressive protein-energy waste, which increases the morbidity and mortality. Most body stores of protein are in skeletal muscle, the protein depletion presents itself as loss of muscle mass, or muscle atrophy. The pathogenesis of muscle wasting is very complex, which is usually caused by multifactors. Previous studies showed that anorexia, activation of the ATP-dependent ubiquitin-proteasome system and defects in insulin/insulin-like growth factor 1 (IGF-1)/PI3K/Akt intracellular signaling processes accelerated muscle protein degradation, decreased protein synthesis, and caused the muscle atrophy. Recent studies found that elevated levels of cytokines, metabolic acidosis, increased levels of myostatin and glucocorticoid also play an important role in causing muscle wasting. Some of their mechanisms are not clear, and more studies are needed for finding effective treatment to improve the outcome of patients with CKD.