当前位置:主页 > 教育论文 > 体育论文 >

肌肉因子与运动对骨骼的作用

发布时间:2018-04-26 15:47

  本文选题:肌肉因子 + 骨代谢 ; 参考:《中国体育科技》2017年06期


【摘要】:肌肉组织已经被认定为内分泌器官,其分泌的活性分子——"肌肉因子"备受关注。从早期胚胎发育到衰老或退化,肌肉和骨骼在形式和功能上都紧密相关,研究肌肉对骨骼的非机械力学作用越来越多。肌肉组织能分泌多种肌肉因子,包括IGF-1、FGF-2、Myostatin、Irisin、IL-6、IL-7、IL-15、BMPs、OGN、FAM5C等。这些分泌因子都对骨组织的各类细胞(如成骨细胞、破骨细胞和软骨细胞)产生不同的作用。运动可以影响肌肉因子的表达水平,进而调控骨代谢。与年龄相关的肌肉衰减(Sarcopenia)和骨质疏松(Osteoporosis)是困扰老年人群健康的两大问题。将肌肉和骨骼视为一个系统,称为肌骨系统,并探讨该系统内部的生物机制可能是解决这些问题的关键所在。进一步揭示肌肉因子介导肌肉和骨骼之间的"Crosstalk"的多条路径,将为运动防治肌肉衰减和骨质疏松提供新的视角。
[Abstract]:Muscle tissue has been recognized as an endocrine organ and its active molecule, muscle factor, has attracted much attention. From early embryonic development to aging or degeneration, muscle and bone are closely related in form and function. Muscle tissue can secrete a variety of muscle factors, including IGF-1 FGF-2, Myostatin, IL-6, IL-7, IL-15, BMPs, OGNN, FAM5C, and so on. These secretory factors have different effects on various kinds of cells in bone tissue, such as osteoblasts, osteoclasts and chondrocytes. Exercise can affect the expression level of muscle factors, and then regulate bone metabolism. Age-related muscle attenuation (Sarcopenia) and osteoporosis (Osteoporosism) are two major health problems for the elderly. Consider muscle and bone as a system called musculoskeletal system and explore the biological mechanism within the system may be the key to solve these problems. Further revealing the multiple pathways of "Crosstalk" between muscle and bone mediated by muscle factors will provide a new perspective for the prevention and treatment of muscle attenuation and osteoporosis by exercise.
【作者单位】: 青少年健康评价与运动干预教育部重点实验室;华东师范大学体育与健康学院;
【分类号】:G804.2;R87

【相似文献】

相关期刊论文 前3条

1 陈苏赣,董榴英;体育运动对中老年人骨代谢的影响[J];上饶师范学院学报(自然科学版);2003年03期

2 孙平;蔡德鸿;黄震;;失重与骨代谢调节失衡[J];中国骨质疏松杂志;2006年05期

3 欧超,刘思金,薛延,杨成燕;运动对绝经后妇女骨量和骨代谢的影响[J];徐州师范大学学报(自然科学版);2000年02期



本文编号:1806656

资料下载
论文发表

本文链接:https://www.wllwen.com/jiaoyulunwen/tylw/1806656.html


Copyright(c)文论论文网All Rights Reserved | 网站地图 |

版权申明:资料由用户d7439***提供,本站仅收录摘要或目录,作者需要删除请E-mail邮箱bigeng88@qq.com