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JCI early table of contents for Feb. 22, 2013
Date:2/22/2013

COMPANYING COMMENTARY

TITLE:
Virgin birth: engineered heart muscle from parthenogenic stem cells

AUTHOR CONTACT:
Michael D. Schneider
Imperial College London, London, UNK, GBR
Phone: 011 44 20 7594 3027; Fax: 011 44 20 7594 3190; E-mail: m.d.schneider@imperial.ac.uk

View this article at: http://www.jci.org/articles/view/67961?key=a07301e0e8f34e261854


Pulmonary fibrosis: between a ROCK and a hard place

Pulmonary fibrosis is a scarring or thickening of the lungs that causes shortness of breath, a dry cough, fatigue, chest discomfort, weight loss, a decrease in the ability of the lungs to transmit oxygen to the blood stream, and, eventually, heart failure. Cells known as myofibroblasts normally secrete materials that are required for wound healing; once the wound has closed, the cells disappear. In pulmonary fibrosis, the myofibroblasts stick around, continuing to secrete wound healing factors that cause fibrosis in the lungs. In this issue of the Journal of Clinical Investigation, Yong Zhou and colleagues at the University of Alabama at Birmingham identified a mechanosensitive cellular signaling pathway in myofibroblasts that is activated by the hardening of tissue that has become fibrotic. Activation of this pathway promotes myofibroblast survival and prevents the normal disappearance of these cells after completion of wound healing. The pathway is dependent on a protein known as ROCK. Zhou and colleagues found that a drug that inhibits ROCK, fasudil, attenuates the pro-survival pathway and causes myofibroblasts to die. Further, fasudil treatment protected mice from injury-induced lung fibrosis. These studies suggest that ROCK inhibitors could be used to treat pulmonary fibrosis. In a companion Attending Physician article,
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Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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