Mechanotransduction in skeletal muscle

被引:96
作者
Burkholder, Thomas J. [1 ]
机构
[1] Georgia Inst Technol, Sch Appl Physiol, Atlanta, GA 30332 USA
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2007年 / 12卷
关键词
skeletal muscle; mechanotransduction; stretch; deformation; signaling pathway; insulin-like growth factor I; IGF-I; AMP kinase; AMPK; mitogen activated protein kinase; MAP; phosphatidylinositol-3 ' kinase; PI-3K; prostaglandins; PG transduction; review;
D O I
10.2741/2057
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Mechanical signals are critical to the development and maintenance of skeletal muscle, but the mechanisms that convert these shape changes to biochemical signals is not known. When a deformation is imposed on a muscle, changes in cellular and molecular conformations link the mechanical forces with biochemical signals, and the close integration of mechanical signals with electrical, metabolic, and hormonal signaling may disguise the aspect of the response that is specific to the mechanical forces. The mechanically induced conformational change may directly activate downstream signaling and may trigger messenger systems to activate signaling indirectly. Major effectors of mechanotransduction include the ubiquitous mitogen activated protein kinase (MAP) and phosphatidylinositol-3' kinase (PI-3K), which have well described receptor dependent cascades, but the chain of events leading from mechanical stimulation to biochemical cascade is not clear. This review will discuss the mechanics of biological deformation, loading of cellular and molecular structures, and some of the principal signaling mechanisms associated with mechanotransduction.
引用
收藏
页码:174 / 191
页数:18
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