METABOLIC AND MOLECULAR ASPECTS OF SARCOPENIA

肌肉减少症的代谢和分子方面

• 批准号: 7721465
• 负责人: TODD CADE
• 金额: $ 0.8万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-02-01 至 2009-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7721465
• 关键词: Complex; Computer Retrieval of Information on Scientific Projects Database; Elderly; Funding; Grant; Human; Institution; Lead; Mass Spectrum Analysis; Metabolic; Metabolic Diseases; Metabolism; Mitochondrial Proteins; Molecular; Motor; Mus; Muscle; Muscle Proteins; Pathogenesis; Pattern; Physiological Processes; Post-Translational Protein Processing; Proteins; Proteome; Quality of life; Research; Research Personnel; Resources; Signal Pathway; Skeletal system; Source; United States National Institutes of Health; base; novel; protein expression; sarcopenia; therapeutic target

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Sarcopenia refers to the loss of skeletal muscle protein mass and function that occurs with advancing age. Sarcopenia impairs motor function, and is associated with dysregulated substrate metabolism and reduced quality of life in the elderly. This chapter outlines several phenotypic alterations that are associated with sarcopenia, and considers several physiologic processes and molecular level signaling pathways that may be dysregulated and involved in the pathogenesis of sarcopenia. The pathogenesis is complex and multifactorial. A better understanding of the underlying mechanisms will help identify potential therapeutic targets, and lead to better treatments for sarcopenia. We are exploring and developing mass spectrometry-based approaches for identifying, characterizing, and quantifying muscle mitochondrial protein expression patterns (proteome) in elderly human muscle, and genetically modified mice. By comparison with mitochondrial protein expression patterns in healthy normal muscle, we propose to discover novel proteins and protein forms (post-translational modifications) that may better characterize the pathogenesis of sarcopenia and muscle-based metabolic disorders in the elderly.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 肌肉减少症是指随着年龄的增长而发生的骨骼肌蛋白质质量和功能。肌肉减少症会损害运动功能，并与底物代谢失调和老年人生活质量降低有关。本章概述了与肌肉减少症相关的几种表型变化，并考虑了几种生理过程和分子水平信号传导途径，这些过程可能失调并参与肌肉减少症的发病机理。 发病机理是复杂而多因素的。对潜在机制有更好的了解将有助于确定潜在的治疗靶标，并为肌肉减少症提供更好的治疗方法。我们正在探索和开发基于质谱的方法，以识别，表征和量化老年人肌肉中的肌肉线粒体蛋白表达模式（蛋白质组）以及转基因的小鼠。通过与健康正常肌肉中的线粒体蛋白表达模式进行比较，我们建议发现新型蛋白质和蛋白质形式（翻译后修饰），这些形式可能更好地表征了老年人中肌肉核心和肌肉基于肌肉的代谢性疾病的发病机理。