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胰岛素抵抗、酸中毒、炎症状态等可导致慢性肾脏病患者骨骼肌萎缩,其主要原因可能与泛素溶酶体系统活性亢进有关。泛素溶酶体系统发挥作用需要3种成分:(1)E1连接酶,起活化泛素的作用;(2)E2连接酶,将活化的泛素转运到需要降解的蛋白质分子上;(3)E3连接酶,发挥将泛素准确转运到靶蛋白的调节作用。肌肉特异性环指蛋白1(MuRF1)和肌肉萎缩盒F蛋白(MAFbx/atrogin-1)是两种重要的骨骼肌特异性E3连接酶,其作用可受多种因子影响。探讨MuRF1、MAFbx/atrogin-1与其调控因子之间的相互作用可为骨骼肌萎缩的防治提供很好的思路。
Insulin resistance, acidosis, inflammatory conditions can lead to skeletal muscle atrophy in patients with chronic kidney disease, the main reason may be related to ubiquitin lysosomal system activity. Ubiquitin lysosomal system needs three components to play a role: (1) E1 ligase, which acts as an activator of ubiquitin; (2) E2 ligase that transports activated ubiquitin to the protein molecule to be degraded; (3) ) E3 ligase, play a regulatory role in the accurate transfer of ubiquitin to the target protein. MuRF1 and MAFbx / atrogin-1 are two important skeletal muscle-specific E3 ligases whose effects can be influenced by a variety of factors. To explore the interaction between MuRF1, MAFbx / atrogin-1 and their regulatory factors may provide a good idea for the prevention and treatment of skeletal muscle atrophy.