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与年龄相关的肌肉质量和力量丧失。

Age-related loss of muscle mass and strength.

作者信息

Goldspink Geoffrey

机构信息

Departments of Surgery, Anatomy and Developmental Biology, University College Medical School, Royal Free Hospital Campus, Hampstead, London NW3 2PF, UK.

出版信息

J Aging Res. 2012;2012:158279. doi: 10.1155/2012/158279. Epub 2012 Mar 8.

DOI:10.1155/2012/158279
PMID:22506111
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3312297/
Abstract

Age-related muscle wasting and increased frailty are major socioeconomic as well as medical problems. In the quest to extend quality of life it is important to increase the strength of elderly people sufficiently so they can carry out everyday tasks and to prevent them falling and breaking bones that are brittle due to osteoporosis. Muscles generate the mechanical strain that contributes to the maintenance of other musculoskeletal tissues, and a vicious circle is established as muscle loss results in bone loss and weakening of tendons. Molecular and proteomic approaches now provide strategies for preventing age-related muscle wasting. Here, attention is paid to the role of the GH/IGF-1 axis and the special role of the IGFI-Ec (mechano growth factor/MGF) which is derived from the IGF-I gene by alternative splicing. During aging MGF levels decline but when administered MGF activates the muscle satellite (stem) cells that "kick start" local muscle repair and induces hypertrophy.

摘要

与年龄相关的肌肉萎缩和身体虚弱加剧是重大的社会经济和医学问题。在追求延长生活质量的过程中，充分增强老年人的力量非常重要，这样他们才能完成日常任务，并防止因骨质疏松而导致骨骼脆弱易骨折。肌肉产生的机械应变有助于维持其他肌肉骨骼组织，而肌肉流失会导致骨质流失和肌腱变弱，从而形成恶性循环。分子和蛋白质组学方法现在为预防与年龄相关的肌肉萎缩提供了策略。在此，人们关注生长激素/胰岛素样生长因子-1（GH/IGF-1）轴的作用以及通过选择性剪接从IGF-I基因衍生而来的IGFI-Ec（机械生长因子/MGF）的特殊作用。在衰老过程中，MGF水平下降，但给予MGF时，它会激活肌肉卫星（干）细胞，从而“启动”局部肌肉修复并诱导肥大。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed8/3312297/6d3ffd354c2b/JAR2012-158279.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed8/3312297/15eba12fd0d9/JAR2012-158279.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed8/3312297/3f29633fb4fd/JAR2012-158279.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed8/3312297/30eb6e3d3393/JAR2012-158279.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed8/3312297/4955e31eca3f/JAR2012-158279.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed8/3312297/6d3ffd354c2b/JAR2012-158279.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed8/3312297/15eba12fd0d9/JAR2012-158279.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed8/3312297/3f29633fb4fd/JAR2012-158279.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed8/3312297/30eb6e3d3393/JAR2012-158279.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed8/3312297/4955e31eca3f/JAR2012-158279.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed8/3312297/6d3ffd354c2b/JAR2012-158279.005.jpg

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