Mechanostasis in Apoptosis and Medicine
Progress in Biophysics and Molecular Biology 106 (2011) 517e524 Contents lists available at ScienceDirect Progress in Biophysics and Molecular Biology journal homepage: www.elsevier.com/locate/pbiomolbio Review Mechanostasis in apoptosis and medicine D.D. Chan a,1, W.S. Van Dyke a, M. Bahls b, S.D. Connell a, P. Critser a, J.E. Kelleher c, M.A. Kramer a, S.M. Pearce a, S. Sharma a, C.P. Neu a,* a Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN 47907, United States b Department of Health and Kinesiology, Purdue University, West Lafayette, IN 47907, United States c School of Mechanical Engineering, Purdue University, West Lafayette, IN 47907, United States article info abstract Article history: Mechanostasis describes a complex and dynamic process where cells maintain equilibrium in response Available online 8 August 2011 to mechanical forces. Normal physiological loading modes and magnitudes contribute to cell prolifera- tion, tissue growth, differentiation and development. However, cell responses to abnormal forces include Keywords: compensatory apoptotic mechanisms that may contribute to the development of tissue disease and Apoptosis pathological conditions. Mechanotransduction mechanisms tightly regulate the cell response through Programmed cell death discrete signaling pathways. Here, we provide an overview of links between pro- and anti-apoptotic Mechanobiology signaling and mechanotransduction signaling pathways, and identify potential clinical applications for Shear stress/strain Mechanotransduction treatments of disease by exploiting mechanically-linked apoptotic pathways. Ó Homeostasis 2011 Elsevier Ltd. All rights reserved. Contents 1. Introduction . .................................................517 2. Mechanostasis: tissues adapt to physical cues . ....................................518 3. Programmed cell death . .................................................519 4. Mechanotransduction and apoptosis . ............................................519 4.1.
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