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Controlling the Mechanical Myofibroblast via SRC: A Potential Drug Discovery Platform

[+] Author Affiliations
W. David Merryman, Joshua D. Hutcheson

Vanderbilt University, Nasvhille, TN

Paper No. SBC2010-19187, pp. 345-346; 2 pages
  • ASME 2010 Summer Bioengineering Conference
  • ASME 2010 Summer Bioengineering Conference, Parts A and B
  • Naples, Florida, USA, June 16–19, 2010
  • Conference Sponsors: Bioengineering Division
  • ISBN: 978-0-7918-4403-8
  • Copyright © 2010 by ASME


Connective tissue makes up a large portion of our bodies, with collagen constituting ∼30% of the protein of connective tissue. Any tissue that undergoes fibrosis, either due to a genetic mutation or with age or use, typically falls into the ubiquitous category of ‘connective tissue fibrosis’. There are multiple potential contributors to connective tissue fibrosis; however, two dominate the literature — mechanical stress/strain and cytokines. Both stimuli lead to activation of fibroblast cells to a myofibroblast phenotype, the cellular hallmark of fibrotic disease. The myofibroblast phenotype is indicated by the expression of smooth muscle α-actin (αSMA), which associates with myosin to form actin-myosin contractile elements and generates intracellular force that is transduced to the ECM via cell membrane integrins.

Copyright © 2010 by ASME



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