cheal tissue decreased with blood flow loss. The hypoxia and ischemia preceded fibrosis of the trachea. The authors therefore suggested that revascularization following lung transplantation might be the key to preventing organ rejection and fibrosis. In an accompanying commentary, Alan Contreras and David Briscoe, from Childrens Hospital Boston, delve further into the problem, suggesting that inflammatory revascularization following ischemia is actually what leads to fibrosis and chronic rejection of the organ.
TITLE: Microvascular destruction identifies murine allografts that cannot be rescued from airway fibrosis
AUTHOR CONTACT:
Mark R. Nicolls
Medical Service (111P), Palo Alto, California, USA.
Phone: (650) 493-5000, ext. 69289; Fax: (650) 849-1942; Email: mnicolls@stanford.edu.
MEDIA CONTACT:
Ruthann Richter
Office of Communications and Public Affairs,
Stanford University, Palo Alto, California, USA.
Phone: (650) 725-8047; E-mail: richter1@stanford.edu.
Kerri Childress
Communications Officer
VA Palo Alto Health Care System, Palo Alto, California, USA.
Email: Kerri.Childress@va.gov.
View the PDF of this article at: https://www.the-jci.org/article.php?id=32311
ACCOMPANYING COMMENTARY
TITLE: Every allograft needs a silver lining
AUTHOR CONTACT:
David M. Briscoe
Childrens Hospital Boston, Boston, Massachusetts, USA
Phone: (617) 355-6129; Fax: (617) 730-0130; E-mail: david.briscoe@childrens.harvard.edu.
View the PDF of this article at: https://www.the-jci.org/article.php?id=34238
METABOLIC DISEASE: On
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