硫酸吲哚酚对肌少症信号通路及CKD患者肌细胞的影响
Effect of Indoxyl-sulfate on Sarcopenia Signaling Pathways and Muscle Cells in Patients with CKD
黄诗琦 1崔师妍 1徐鹏昊 1姜晨1
作者信息
- 1. 天津中医药大学第一附属医院(国家中医针灸临床医学研究中心) 天津 300381
- 折叠
摘要
肌少症是慢性肾脏病(chronic kidney disease,CKD)患者常见的并发症之一,主要是由蛋白质摄入不足、活动量减少、慢性炎症等原因导致的肌肉质量、重量及功能异常,最终导致肌肉萎缩的一类临床并发症.硫酸吲哚酚(indoxyl-sulfate,IS)作为蛋白结合性尿毒症毒素,不易通过临床药物及肾脏替代治疗去除,其能通过调控各信号因子,影响多条肌少症通路及机制对骨骼肌细胞造成损害.本文通过总结肌少症主要信号通路及机制,探讨IS是如何导致线粒体功能障碍、骨骼肌细胞萎缩、纤维化等病理情况,从而导致CKD患者肌少症.
Abstract
Sarcopenia is one of the common complications in patients with chronic kidney disease(CKD),it is mainly a clinical complication of muscle mass,weight and function abnormalities and muscle atrophy caused by insufficient protein intake,reduced activity and chronic inflammation.Indoxyl-sulfate(IS),as a protein-bound uremic toxin,is not easy to be removed by clinical drugs and renal replacement therapy,it can affect multiple sarcopenic pathways and mechanisms by regulating various signaling factors and cause damage to skeletal muscle cells.This article summarized the main signaling pathways and mechanisms of sarcopenia,and explored how IS leads to mitochondrial dysfunction,skeletal muscle cell atrophy,fibrosis and other pathological conditions,leading to sarcopenia in CKD patients.By summarizing the main signaling pathways and mechanisms of sarcopenia,this paper explores how IS causes mitochondrial dysfunction,skeletal muscle cell atrophy and fibrosis.
关键词
肌少症/硫酸吲哚酚/慢性肾脏病/肌细胞/信号通路Key words
Sarcopenia/Indoxyl-sulfate/Chronic kidney disease/Muscle cells/Signaling pathways引用本文复制引用
出版年
2024
国家科技期刊平台
NSTL
万方数据