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Science 302 (5644): 406-407

Copyright © 2003 by the American Association for the Advancement of Science

MEDICINE:
PPARs as Therapeutic Targets: Reverse Cardiology?

Jorge Plutzky

Formation of the atherosclerotic lesions that lead to myocardial infarction is determined in part by inflammatory responses such as the production of lipid-laden macrophages. In his Perspective, Plutzky highlights the parts played by PPAR nuclear receptors, especially PPAR-delta (Lee et al.), in the modulation of inflammatory responses and hence atherosclerosis.


The author is in the Department of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA. E-mail: jplutzky{at}rics.bwh.harvard.edu


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
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Y. Takata, J. Liu, F. Yin, A. R. Collins, C. J. Lyon, C.-H. Lee, A. R. Atkins, M. Downes, G. D. Barish, R. M. Evans, et al. (2008)
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The Peroxisome Proliferator Activated Receptor-{gamma} Agonist Pioglitazone Increases Number and Function of Endothelial Progenitor Cells in Patients With Coronary Artery Disease and Normal Glucose Tolerance.
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Preventing type 2 diabetes and cardiovascular disease in metabolic syndrome: the role of PPAR{alpha}.
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Ciprofibrate stimulates the gastrin-producing cell by acting luminally on antral PPAR-{alpha}.
T. C. Martinsen, I. Bakke, D. Chen, A. K. Sandvik, K. Zahlsen, T. Aamo, and H. L. Waldum (2005)
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Activation of Peroxisome Proliferator-Activated Receptor {alpha} by Substituted Urea-Derived Soluble Epoxide Hydrolase Inhibitors.
X. Fang, S. Hu, T. Watanabe, N. L. Weintraub, G. D. Snyder, J. Yao, Y. Liu, J. Y.-J. Shyy, B. D. Hammock, and A. A. Spector (2005)
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Oxidative Stress and Peroxisome Proliferator-Activated Receptors: Reversing the Curse?.
P. R. Devchand, O. Ziouzenkova, and J. Plutzky (2004)
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