JCI online early table of contents: De... (ing Idiopathic pulmonary fibrosis (...)

JCI online early table of contents: Dec. 6, 2010

Date:12/6/2010

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Idiopathic pulmonary fibrosis (IPF) is a chronic lung disorder for which there are currently no treatments. It is a progressive disease that results in lung scarring and changes in lung architecture, which together lead to loss of lung function and death. Although the cause(s) of IPF is unclear, dysregulated signaling triggered by the molecule TGF-beta is known to have a role in disease development. Parviz Minoo, Zea Borok, and colleagues, at the University of Southern California, Los Angeles, have now been able to more specifically pinpoint the role of dysregulated TGF-beta signaling in disease development using a mouse model of lung fibrosis (scarring).

The researchers generated mice lacking T-beta-RII the molecule to which TGF-beta binds to trigger a signaling cascade on cells lining the lung (epithelial cells). Importantly, these mice showed increased survival and resistance to fibrosis in the chemical-induced model of fibrosis studied. The authors therefore suggest that T-beta-RII could provide a new target for the development of therapeutics to treat IPF.

TITLE: Epithelium-specific deletion of TGF-beta receptor type II protects mice from bleomycin-induced pulmonary fibrosis

AUTHOR CONTACT:
Parviz Minoo
University of Southern California, Los Angeles, California, USA.
Phone: 323.226.4340; Fax: 213.236.5049; E-mail: minoo@usc.edu.

Zea Borok
Keck School of Medicine of the University of Southern California, Los Angeles, California, USA.
Phone: 323.226.7923; Fax: 323.226.2738; E-mail: zborok@usc.edu.

View this article at: http://www.jci.org/articles/view/42090?key=5b106d2bdee99290407d

MUSCLE BIOLOGY: Linking two previously disparate muscle diseases

Individuals with mutations in their DES gene have
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Contact: Karen Honey
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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