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Atherosclerosis, a common disease of the cardiovascular system in which fatty material is deposited in the walls of arteries and causes narrowing of the vessels gradually impairing blood flow. Finding a way to stop this process of fatty deposition would be a major medical breakthrough, thus understanding the molecular mechanisms by which it happens are an essential line of study.
Using a transgenic mouse model, researchers at Vanderbilt University Medical Center in Nashville showed that the adipocyte fatty acid binding protein, aP2, is an essential part of the inflammation that takes place in atherosclerosis. aP2 is expressed by immune cells called macrophages (Nature Medicine, Vol. 7, No. 6, 01 Jun 2001). Mice that are prone to atherosclerosis but which lack the aP2 gene are protected against the disease and are otherwise apparently normal. Thus, aP2 presents a new therapeutic target for the prevention of atherosclerosis. CONTACT: Dr. MacRae Linton
Department of Medicine
Vanderbilt University Medical Center
Nashville, TN
USA
Tel: +1 615-936-1450
Fax: +1 615-936-1872
Email: macrae.linton@mcmail.vanderbilt.edu (C) Nature Medicine press release.
Message posted by: Trevor M. D'Souza
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