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

骨骼肌无力和消瘦是危重病的常见并发症，与预后不良和长期留在重症监护室（ICU）有关;这被称为ICU获得性轻瘫（ICUAP）。原因尚不完全清楚，但据认为有许多因素，包括感染，药物和不动。FHL 1和肌肉生长抑制素是在肌肉质量的调节中重要的蛋白质，并且它们本身由肌肉活动调节。目前尚不清楚它们是否对人类ICUAP的发展很重要，但根据目前的科学证据，我们相信它们会很重要。本项目旨在研究这些蛋白质的作用及其在ICUAP中的重要性。通过实验室和ICU中真实的患者的实验，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提供目标。

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.