When a blood vessel becomes blocked, the tissue that it serves experiences ischemia—a state of low oxygen supply—that slowly kills the tissue. If and when blood flow returns (reperfusion), it can often cause even greater damage to the tissue. This type of ischemia/reperfusion (IR) injury occurs in heart attacks, and understanding the mechanisms involved in IR could lead to the development of new drugs to save damaged tissue and treat heart attack.
Using a mouse lung model of IR, David Stern and colleagues at Columbia University, have now discovered that one molecule unifies many of the pathways that lead to IR tissue damage (Nature Medicine, Vol. 6, Issue 12, 01 Dec 2000). The scientists stopped blood flow to the lungs for 60 minutes and then reperfused them for 3 hours. They saw that levels of the Early growth response (Egr-1) gene were elevated substantially during IR. They also demonstrated that Egr-1 is the common link between the diverse pathways that cause tissue injury, such as the stimulation of chemokines, adhesion receptor molecules, procoagulants, and permeability-related genes. Deleting the Egr-1 gene decreased tissue injury and enhanced animal survival and organ function.
These studies show that Egr-1 plays a central role in ischemic tissue damage, and suggest that Egr-1 may be a good drug target for the treatment of ischemic conditions.
Dr David M Stern
Department of Surgery
College of Physicians & Surgeons of Columbia University
630 West 168th Street
New York, NY, 10032
Tel: +1 212 305 1615
Fax: +1 212 305 5337
(C) Nature Medicine press release
Message posted by: Trevor M. D'Souza