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慢性肾脏病(CKD)患者常伴难纠正的进行性蛋白-能量消耗(PEW),临床主要表现骨骼肌萎缩。肌萎缩的发病机制很复杂,常由多因素共同作用所致。既往研究认为食欲减退、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/磷脂酰肌醇激酶/蛋白激酶B信号通路受损是导致肌萎缩的主要原因。然而随着近年大量深入研究,发现炎症反应、代谢性酸中毒、激素代谢紊乱和肌抑素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,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。
Patients with chronic kidney disease (CKD) often have difficult-to-correct progressive protein-energy expenditure (PEW) and clinically manifest skeletal muscle atrophy. The pathogenesis of muscle atrophy is very complicated, often caused by multiple factors together. Previous studies suggest that loss of appetite, activation of the ubiquitin-protease system, and impaired intracellular insulin / insulin-like growth factor 1 / phosphatidylinositol kinase / protein kinase B signaling are the major causes of muscle atrophy. However, with the extensive and intensive researches in recent years, it is found that inflammation, metabolic acidosis, disorders of hormone metabolism and increased expression of myostatin may play an important role in the development of muscle atrophy. However, some of these mechanisms have not yet been fully elucidated , Need to explore in-depth, in order to find practical and effective intervention target, to improve the clinical prognosis of patients with CKD.