Abstract
Purpose of review The bioactive lysophospholipids, lysophosphatidic acid (LPA) and sphingosine 1 phosphate (S1P), have potent effects on blood and vascular cells. This review focuses their potential contributions to the development of atherosclerosis, acute complications such as acute myocardial infarction, and chronic ischemic cardiac damage. Recent findings Exciting recent developments have provided insight into the molecular underpinnings of LPA and S1P receptor signaling. New lines of evidence suggest roles for these pathways in the development of atherosclerosis. In experimental animal models, the production, signaling, and metabolism of LPA may be influenced by environmental factors in the diet that synergize to promote the progression of atherosclerotic vascular disease. This is supported by observations of human polymorphisms in the lysophospholipidmetabolizing enzyme PPAP2B, which are associated with risk of coronary artery disease and myocardial infarction. S1P signaling protects from myocardial damage that follows acute and chronic ischemia, both by direct effects on cardiomyocytes and through stem cell recruitment to ischemic tissue. Summary This review will suggest novel strategies to prevent the complications of coronary artery disease by targeting LPA production and signaling. Additionally, ways in which S1P signaling pathways may be harnessed to attenuate ischemia-induced cardiac dysfunction will be explored.
Original language | English |
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Pages (from-to) | 432-437 |
Number of pages | 6 |
Journal | Current Opinion in Lipidology |
Volume | 26 |
Issue number | 5 |
DOIs | |
State | Published - Oct 2015 |
Bibliographical note
Publisher Copyright:Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Funding
This project was supported by grants from the Heart Lung and Blood Institute (R01HL120507 and R56HL124266), the National Center for Research Resources (P20RR021954), an IDeA award from the National Institute of General Medical Sciences (P20GM103527), and the National Center for Advancing Translational Sciences through Grant UL1TR000117 of the National Institutes of Health. This material is the result of work supported in part with resources and the use of facilities at the Lexington VA Medical Center (through awards BX002769 and BX001014). This project was supported by grants from the Heart Lung and Blood Institute (R01HL120507 and R56HL124266), the National Center for Research Resources (P20RR021954), an IDeA award fromthe National Institute of General Medical Sciences (P20GM103527), and the National Center for Advancing Translational Sciences through Grant UL1TR000117 of the National Institutes of Health. This material is the result of work supported in part with resources and the use of facilities at the Lexington VA Medical Center (through awards BX002769 and BX001014).
Funders | Funder number |
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National Heart, Lung, and Blood Institute (NHLBI) | R01HL120507, R56HL124266 |
Durham VA Medical Center | BX002769, BX001014 |
National Institutes of Health (NIH) | |
National Institute of General Medical Sciences | P20GM103527 |
National Center for Research Resources | P20RR021954 |
U.S. Department of Veterans Affairs | I01BX002769 |
National Center for Advancing Translational Sciences (NCATS) | UL1TR000117 |
Keywords
- Autotaxin
- Lysophosphatidic acid
- Sphingosine 1 phosphate
- Sphingosine kinase
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Molecular Biology
- Genetics
- Nutrition and Dietetics
- Cardiology and Cardiovascular Medicine
- Cell Biology