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JCI early table of contents for Nov. 19, 2012
Date:11/19/2012


Loss of KLF4 promotes atherosclerosis in mice

Atherothrombosis, or the formation of a clot in an artery, is one of the major causes of heart attack, stroke, and peripheral artery disease. Clot formation is primarily regulated by the endothelium, the cells which line the insides of the arteries and veins. Previously, researchers led by Mukesh Jain at Case Western Reserve University identified KLF4 as a protective factor that was induced by blood flow and was associated with reduced clot formation. In this issue of the Journal of Clinical Investigation, Jain and colleagues examined atherosclerotic plaque formation in KLF4 mutant mice fed a high fat diet. They found that mice lacking KLF4 had significantly enhanced atherosclerosis compared to normal mice, while mice with extra KLF4 had reduced atherosclerosis. These results establish KLF4 as a key regulator of atherothrombosis.

TITLE:
Endothelial Kruppel-like factor 4 protects against atherothrombosis in mice

AUTHOR CONTACT:
Mukesh Jain
Case Western Reserve University, Cleveland, OH, USA
Phone: 216-368-3607; E-mail: mukesh.jain2@case.edu

View this article at: http://www.jci.org/articles/view/66056?key=f81438bdf96cff1c94ff


Mutation in SH2B1 linked to obesity

The protein SH2B1 interacts with cell surface receptors that mediate signaling by insulin and leptin, two hormones that are associated with obesity. Mice lacking Sh2b1 exhibit increased food intake, obesity, and insulin resistance. In a study published in the Journal of Clinical Investigation, researchers led by Sadaf Farooqi at Addenbrooke's Hospital in Cambridge, England identified a mutation in SH2B1 in a group of patients with severe early onset diabetes. These patients had increased food intake, early childhood obesity, insu
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Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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