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Arguing the case for the autotaxin-lysophosphatidic acid-lipid phosphate phosphatase 3-signaling nexus in the development and complications of atherosclerosis. | LitMetric

Arguing the case for the autotaxin-lysophosphatidic acid-lipid phosphate phosphatase 3-signaling nexus in the development and complications of atherosclerosis.

Arterioscler Thromb Vasc Biol

From the Veterans Affairs Medical Center, Cardiovascular Medicine Service, Lexington, KY (S.S.S., A.J.M.); and Division of Cardiovascular Medicine, Gill Heart Institute, University of Kentucky, Lexington, KY (S.S.S., P.M., F.Y., J.A.B., A.J.M.).

Published: March 2014

AI Article Synopsis

Article Abstract

The structurally simple glycero- and sphingo-phospholipids, lysophosphatidic acid (LPA) and sphingosine-1-phosphate, serve as important receptor-active mediators that influence blood and vascular cell function and are positioned to influence the events that contribute to the progression and complications of atherosclerosis. Growing evidence from preclinical animal models has implicated LPA, LPA receptors, and key enzymes involved in LPA metabolism in pathophysiologic events that may underlie atherosclerotic vascular disease. These observations are supported by genetic analysis in humans implicating a lipid phosphate phosphatase as a novel risk factor for coronary artery disease. In this review, we summarize current understanding of LPA production, metabolism, and signaling as may be relevant for atherosclerotic and other vascular disease.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3944085PMC
http://dx.doi.org/10.1161/ATVBAHA.113.302737DOI Listing

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