Inactivity and inflammation: selected cytokines as biologic mediators in muscle dysfunction during critical illness.

Chris Winkelman
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引用次数: 76

Abstract

Muscle dysfunction leads to activity intolerance, prolonged hospitalization, and additional days of mechanical ventilation. The etiology of muscle dysfunction in the critically ill patient is multifactoral. Inactivity and inflammation, common phenomena to patients in the intensive care unit, are associated with myopathy and muscle dysfunction. Cytokines are small biological active molecules that regulate inflammation and have a direct effect on muscle wasting. The purpose of this article is to describe selected cytokines (ie, interleukin-1, interleukin-6, interleukin-10, and tumor necrosis factor), explain their role in muscle dysfunction, and explore the role of therapeutic activity as a moderator of muscle dysfunction and cytokine-mediated muscle damage.

不活动和炎症:选择细胞因子作为危重疾病期间肌肉功能障碍的生物介质。
肌肉功能障碍导致活动不耐受、住院时间延长和机械通气天数增加。危重病人肌肉功能障碍的病因是多因素的。不活动和炎症是重症监护病房患者的常见现象,与肌病和肌肉功能障碍有关。细胞因子是调节炎症的小生物活性分子,对肌肉萎缩有直接影响。本文的目的是描述选定的细胞因子(即白细胞介素-1、白细胞介素-6、白细胞介素-10和肿瘤坏死因子),解释它们在肌肉功能障碍中的作用,并探讨治疗活性在肌肉功能障碍和细胞因子介导的肌肉损伤中的调节作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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