Does FHL 1 enhanced myostatin activity mediate intensive care unit acquired paresis ?

骨骼肌无力和消瘦是危重症的常见并发症，与预后不良和在重症监护病房（ICU）的住院时间延长有关；这被称为ICU获得性轻瘫（ICUAP）。病因尚不完全清楚，但据认为有许多因素，包括感染、药物和不活动。FHL1和肌肉生长抑制素是调节肌肉质量的重要蛋白质，它们本身受肌肉活动的调节。目前尚不清楚它们在人类ICUAP的发展中是否重要，但根据目前的科学证据，我们相信它们是重要的。本项目旨在探讨这些蛋白在ICUAP中的作用及其重要性。通过实验室实验和ICU的真实患者，我们将验证我们的理论，即它们相互作用，在ICUAP的发展中很重要。通过这项研究，我们希望能够更好地了解导致这一问题的因素，并为潜在的治疗方法找到目标。

Skeletal muscle weakness and wasting is a common complication of critical illness and is associated with a poor outcome and prolonged stay on intensive care units (ICU); this is known as ICU acquired paresis (ICUAP). The causes are not fully understood, but it is thought that many factors contribute, including infection, medications and immobility. FHL1 and myostatin are proteins that are important in the regulation of muscle mass and are themselves regulated by muscle activity. It is not known if they are important in the development of ICUAP in humans but, based on current scientific evidence, we believe that they will be. This project aims to investigate the roles of these proteins and their importance in ICUAP. With experiments in the laboratory and in real patients on ICU we will test our theory that they interact together and are important in the development of ICUAP. With this study we hope to be able to better understand the factors leading to this problem and generate target for potential treatments.