doi: 10.1161/CIRCRESAHA.107.170233
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© 2008 American Heart Association, Inc.
Editorials |
Peroxisome Proliferator-Activated Receptor β/
Goes Vascular
From Translational Medicine and Therapeutics, William Harvey Research Institute, Barts and the London, Queen Mary University London, UK.
Correspondence to David Bishop-Bailey, Translational Medicine and Therapeutics, William Harvey Research Institute, Barts and the London, Queen Mary University London, Charterhouse Square, London EC1M 6BQ, United Kingdom. E-mail d.bishop-bailey@qmul.ac.uk
See related article, pages 193–200
Key Words: PPAR • vascular smooth muscle • endothelial cell • TGFβ
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Peroxisome proliferator-activated receptor (PPAR)s are a family of 3 (PPAR
, -β/
, and -
) nuclear receptor/ligand-activated transcription factors that work in concert as heterodimers with the retinoid X receptors.1 In recent years, there has been great scientific and clinical interest in the actions of PPAR and PPAR because they are the molecular targets for the clinically used lipid-lowering fibrates and insulin-sensitizing thiazolidinedione classes of drugs, respectively.2 Until recently, very little has been known about the cellular roles of PPAR, even though it is by far the most ubiquitously expressed of the PPAR receptors.1,3 The recent development of highly selective ligands and PPARβ/ knockout and transgenic mice, however, have now implicated roles for PPARβ/ in adipose tissue formation, metabolism, wound healing, brain development, placental function, colorectal carcinogenesis, and skeletal muscle function.4–6 PPARβ/ ligands appear highly effective in regulating lipid metabolism, particularly in skeletal muscle,7,8 and are currently in phase II clinical trials for treatment of dyslipidemia, aimed particularly at individuals with low HDL levels.
All of the PPARs, therefore, appear to be able to target aspects of the metabolic syndrome.6 Because the metabolic syndrome represents a major risk factor for cardiovascular diseases, there has been an increasing interest in the roles of PPARs, in particular most recently PPARβ/, in vascular biology. Indeed, in addition to the treatment of dyslipidemia, PPARβ/ ligands may reduce the development in atherosclerosis in the high-fat Western diet LDL receptor–/– mouse model.9,10 A similar study using adoptive transfer of PPARβ/–/– monocytes in to
Related Article:
Circ. Res. 2008 102: 193-200.
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  L. Piqueras, M. J. Sanz, M. Perretti, E. Morcillo, L. Norling, J. A. Mitchell, Y. Li, and D. Bishop-Bailey Activation of PPAR{beta}/{delta} inhibits leukocyte recruitment, cell adhesion molecule expression, and chemokine release J. Leukoc. Biol., July 1, 2009; 86(1): 115 - 122. [Abstract] [Full Text] [PDF]
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