METABOLIC AND MOLECULAR ASPECTS OF SARCOPENIA

肌肉减少症的代谢和分子方面

• 批准号: 7355277
• 负责人: TODD CADE
• 金额: $ 0.85万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-02-01 至 2007-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7355277
• 关键词: METABOLIC; MOLECULAR; ASPECTS; SARCOPENIA

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.

该子项目是利用 NIH/NCRR 资助的中心拨款提供的资源的众多研究子项目之一。子项目和研究者 (PI) 可能已从另一个 NIH 来源获得主要资金，因此可以在其他 CRISP 条目中出现。列出的机构是中心的机构，不一定是研究者的机构。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的丧失。肌肉减少症会损害运动功能，并与老年人的底物代谢失调和生活质量下降有关。本章概述了与肌肉减少症相关的几种表型改变，并考虑了可能失调并参与肌肉减少症发病机制的几种生理过程和分子水平信号通路。其发病机制复杂，涉及多因素。更好地了解潜在机制将有助于确定潜在的治疗靶点，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，用于识别、表征和量化老年人肌肉和转基因小鼠的肌肉线粒体蛋白表达模式（蛋白质组）。通过与健康正常肌肉中的线粒体蛋白表达模式进行比较，我们建议发现新的蛋白质和蛋白质形式（翻译后修饰），它们可以更好地表征老年人肌少症和肌肉代谢紊乱的发病机制。