Skip to main content Accessibility help
×
Hostname: page-component-78c5997874-ndw9j Total loading time: 0 Render date: 2024-11-18T15:05:53.985Z Has data issue: false hasContentIssue false

19 - Summary and Outlook

Published online by Cambridge University Press:  05 July 2014

Mohammad R. K. Mofrad
Affiliation:
University of California, Berkeley
Roger D. Kamm
Affiliation:
Massachusetts Institute of Technology
Mohammad R. K. Mofrad
Affiliation:
University of California, Berkeley
Roger D. Kamm
Affiliation:
Massachusetts Institute of Technology
Get access

Summary

Introduction

The primary objective of this book was to bring together various points of view on cellular mechanotransduction. This final, closing chapter attempts to summarize the various viewpoints discussed in previous chapters and establish a horizon for future research directions toward understanding the underlying processes involved in mechanotransduction.

Mechanotransduction is an essential function of the cell, controlling its growth, proliferation, protein synthesis, and gene expression. Extensive data exist documenting the cellular responses to external forces, but less is known about how force affects biological signaling. More generally, the question of how the mechanical and biochemical pathways interact remains largely unanswered. As articulated in the various chapters of this book, many studies during the past two decades have been carried out to shed light on a wide range of cellular responses to mechanical stimulation. It is well known that living cells can sense mechanical stimuli, and that forces applied to a cell or physical cues from the extracellular environment can elicit a wide range of biochemical responses that affect the cell’s phenotype in health and disease. It is now widely accepted that stresses experienced in vivo are instrumental in a wide spectrum of pathologies. One of the first diseases found to be linked to cellular stress was atherosclerosis, where it was demonstrated that hemodynamic shear influences endothelial function and that conditions of low or oscillatory shear stress are conducive to the formation and growth of atherosclerotic lesions. Similarly, the disease process of calcification in heart valves can be understood as a mechanotransduction phenomenon as valvular endothelial and interstitial cells tend to respond to pathophysiological stresses from disturbed blood flow patterns directly linked with abnormal deformations in the valve tissue. The role of mechanical stress on bone growth and healing was probably the first to be widely recognized, and since then many other stress-influenced cell functions have been identified.

Type
Chapter
Information
Cellular Mechanotransduction
Diverse Perspectives from Molecules to Tissues
, pp. 438 - 444
Publisher: Cambridge University Press
Print publication year: 2009

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

Save book to Kindle

To save this book to your Kindle, first ensure coreplatform@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×