4.5 Review

Mechanotransduction in skeletal muscle

Journal

FRONTIERS IN BIOSCIENCE-LANDMARK
Volume 12, Issue -, Pages 174-191

Publisher

FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/2057

Keywords

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

Funding

  1. NIAMS NIH HHS [AR 48664, AR48884, R01 AR048884, R55 AR048664-01] Funding Source: Medline

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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.

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