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Researchers discover a new pathway in blood vessel inflammation and disease
Date:9/4/2013

ared mainly in smooth muscle cells and that levels were markedly reduced in atherosclerotic human blood vessels. To establish causality, the team generated genetically-modified mice where they deleted KLF-15 gene in smooth muscle cells.

"We expected to see more proliferation of the smooth muscle cells as this is a common response of this cell type in disease," Lu said, first author on the paper. "Instead, we were surprised to see rampant vascular inflammation and hyper activated NF-kB, the master regulator of inflammation."

The results offer hope for the development of specific anti-inflammatory therapies for vascular disease. Cholesterol-lowering drugs such as statins have some anti-inflammatory effects, but despite their widespread use, the burden of vascular disease remains high. As statins' primary role is to lower cholesterol levels, developing additional or more potent anti-inflammatory therapies are needed to compliment statins' important function.

Jain's previous research of the KLF family of genetic factors revealed regulator functions in blood vessels. KLF4 was shown to potently inhibit inflammation in the endothelium, the other major cell type in vessels. The current work is first to establish a role for these factors in smooth muscle inflammation.

"Collectively, these studies establish KLFs as a central hub regulating vascular health," Jain said. "Boosting levels of these factors may be a particularly effective way to reduce inflammation and the development or progression of vascular diseases such as atherosclerosis."


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Contact: Jessica Studeny
jes91@case.edu
216-368-4692
Case Western Reserve University
Source:Eurekalert

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