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肌萎缩蛋白-1(Atrogin-1)、泛素连接酶 E3 家族成员 1(MuRF-1)与肌肉减少症。

Atrogin-1, MuRF-1, and sarcopenia.

机构信息

Department of Orthopaedic Surgery, University of Michigan Medical School, 109 Zina Pitcher Place, BSRB 2017, Ann Arbor, MI, 48109-2200, USA.

出版信息

Endocrine. 2013 Feb;43(1):12-21. doi: 10.1007/s12020-012-9751-7. Epub 2012 Jul 20.

Abstract

Sarcopenia is one of the leading causes of disability in the elderly. Despite the growing prevalence of sarcopenia, the molecular mechanisms that control aging-related changes in muscle mass are not fully understood. The ubiquitin proteasome system is one of the major pathways that regulate muscle protein degradation, and this system plays a central role in controlling muscle size. Atrogin-1 and MuRF-1 are two E3 ubiquitin ligases that are important regulators of ubiquitin-mediated protein degradation in skeletal muscle. In this review, we will discuss: (i) aging-related changes to skeletal muscle structure and function; (ii) the regulation of protein synthesis and protein degradation by IGF-1, TGF-β, and myostatin, with emphasis on the control of atrogin-1 and MuRF-1 expression; and (iii) the potential for modulating atrogin-1 and MuRF-1 expression to treat or prevent sarcopenia.

摘要

肌肉减少症是老年人残疾的主要原因之一。尽管肌肉减少症的患病率不断上升,但控制肌肉质量与衰老相关变化的分子机制尚不完全清楚。泛素蛋白酶体系统是调节肌肉蛋白降解的主要途径之一,它在控制肌肉大小方面起着核心作用。Atrogin-1 和 MuRF-1 是两种 E3 泛素连接酶,它们是骨骼肌中泛素介导的蛋白降解的重要调节因子。在这篇综述中,我们将讨论:(i)与衰老相关的骨骼肌结构和功能变化;(ii)IGF-1、TGF-β 和肌肉生长抑制素对蛋白质合成和蛋白质降解的调节,重点是控制 Atrogin-1 和 MuRF-1 的表达;以及(iii)调节 Atrogin-1 和 MuRF-1 表达以治疗或预防肌肉减少症的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43e4/3586538/0d91900e854f/nihms-444555-f0001.jpg

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