Mechanotransduction: the role of mechanical stress, myocyte shape, and cytoskeletal architecture on cardiac function

被引:163
|
作者
McCain, Megan L. [1 ,2 ]
Parker, Kevin Kit [1 ,2 ]
机构
[1] Harvard Univ, Sch Engn & Appl Sci, Cambridge, MA 02138 USA
[2] Harvard Univ, Dis Biophys Grp, Wyss Inst Biol Inspired Engn, Cambridge, MA 02138 USA
来源
关键词
Mechanotransduction; Heart; Cytoskeleton; Cardiac sarcomere; Cardiac myocytes; Mechanosensitivity; DYSTROPHIN-GLYCOPROTEIN COMPLEX; EXTRACELLULAR-MATRIX COMPONENTS; RIGHT-VENTRICULAR HYPERTROPHY; STRETCH-INDUCED HYPERTROPHY; ADULT-RAT CARDIOMYOCYTES; ACTION-POTENTIAL CHANGES; CELL-CELL ADHESION; BETA 1D INTEGRIN; N-CADHERIN; MYOCARDIAL-INFARCTION;
D O I
10.1007/s00424-011-0951-4
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Mechanotransduction refers to the conversion of mechanical forces into biochemical or electrical signals that initiate structural and functional remodeling in cells and tissues. The heart is a kinetic organ whose form changes considerably during development and disease, requiring cardiac myocytes to be mechanically durable and capable of fusing a variety of environmental signals on different time scales. During physiological growth, myocytes adaptively remodel to mechanical loads. Pathological stimuli can induce maladaptive remodeling. In both of these conditions, the cytoskeleton plays a pivotal role in both sensing mechanical stress and mediating structural remodeling and functional responses within the myocyte.
引用
收藏
页码:89 / 104
页数:16
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