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.
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ASME 2010 Summer Bioengineering Conference
June 16–19, 2010
Naples, Florida, USA
Conference Sponsors:
- Bioengineering Division
ISBN:
978-0-7918-4403-8
PROCEEDINGS PAPER
Controlling the Mechanical Myofibroblast via SRC: A Potential Drug Discovery Platform Available to Purchase
W. David Merryman,
W. David Merryman
Vanderbilt University, Nasvhille, TN
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Joshua D. Hutcheson
Joshua D. Hutcheson
Vanderbilt University, Nasvhille, TN
Search for other works by this author on:
W. David Merryman
Vanderbilt University, Nasvhille, TN
Joshua D. Hutcheson
Vanderbilt University, Nasvhille, TN
Paper No:
SBC2010-19187, pp. 345-346; 2 pages
Published Online:
July 15, 2013
Citation
Merryman, WD, & Hutcheson, JD. "Controlling the Mechanical Myofibroblast via SRC: A Potential Drug Discovery Platform." Proceedings of the ASME 2010 Summer Bioengineering Conference. ASME 2010 Summer Bioengineering Conference, Parts A and B. Naples, Florida, USA. June 16–19, 2010. pp. 345-346. ASME. https://doi.org/10.1115/SBC2010-19187
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