Opposites Attract: The Protein Apelin Counters The Effects Of Ang II In Diseases Of The Major Arterial Blood Vessels
Main Category: Cardiovascular / CardiologyArticle Date: 04 Sep 2008 - 4:00 PDT
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One of the most common causes of death in the developed world is a disease of the major arterial blood vessels that can cause heart attacks and stroke. New insight into the molecular pathways involved in this disease (which is known as atherosclerosis, or hardening of the arteries) and another disease of the main arterial blood vessel leaving the heart (abdominal aortic aneurysm [AAA]) has been provided by Thomas Quertermous and colleagues, at Stanford University School of Medicine, who studied a mouse model of these diseases - the ApoE-KO mouse.
In the study, administration of the hormone Ang II to ApoE-KO mice induced atherosclerosis and the formation of AAA. The effects of Ang II could be inhibited by coinfusion of another natural molecule, apelin. Further analysis indicated that apelin inhibited the effects of Ang II by increasing production of a molecule known as NO and by blocking Ang II-initiated signaling (in part through the interaction of the receptor for apelin and the receptor for Ang II). These data identify a mechanism whereby the ability of Ang II to cause diseases of the major arterial blood vessels can be countered, information that is likely to be of interest to those developing therapeutics for these diseases.
TITLE: Apelin signaling antagonizes Ang II effects in mouse models of atherosclerosis
AUTHOR:
Thomas Quertermous
Stanford University School of Medicine, Stanford, California, USA.
http://www.stanford.edu
View the PDF of this article at: https://www.the-jci.org/article.php?id=34871
Source:
Karen Honey
Journal of Clinical Investigation
Visit our cardiovascular / cardiology section for the latest news on this subject.
MLA
14 Feb. 2012. <http://www.medicalnewstoday.com/releases/120205.php>
APA
http://www.medicalnewstoday.com/releases/120205.php.
Please note: If no author information is provided, the source is cited instead.
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