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(Circulation Research. 2008;103:7.)
© 2008 American Heart Association, Inc.

Editorials

Endothelial Progenitor Cells and Angiogenesis Join the PPARty

Federico Biscetti, Roberto Pola

From the Laboratory of Vascular Biology and Genetics, Department of Medicine (F.B., R.P.), A. Gemelli University Hospital, Catholic University School of Medicine, Rome, Italy; the Department of Anatomy and Cell Biology (R.P.), Tufts University School of Medicine, Boston, Mass; and IRCCS OASI (R.P.), Torina, Italy.

Correspondence to Roberto Pola, MD, PhD, Department of Anatomy and Cell Biology, Tufts University School of Medicine, 136 Harrison Avenue, 02111 Boston, MA 02155. E-mail roberto.pola@tufts.edu

See related article, pages 80–88

Key Words: endothelial progenitor cells • angiogenesis • prostacyclin • PPARs

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Peroxisome proliferator-activated receptors (PPARs) are ligand-inducible transcription factors that belong to the nuclear hormone receptor superfamily.¹ In mammals, the PPAR family consists of 3 subtypes of proteins encoded by separate genes: PPAR (NR1C1), PPAR (NR1C3), and PPAR (also known as β or NR1C2).² They act as heterodimers with the retinoid X receptor and regulate gene transcription by binding to specific response elements in the promoter of the target genes.³ The classical biological activity of PPAR is the regulation of the rate of fatty acid uptake and their esterification into triglyceride or oxidation,^4–7 whereas PPAR is classically involved in adipocyte differentiation, regulation of fat storage, and maintenance of glucose homeostasis.⁵ The physiological functions of PPAR are instead still unclear, although it is known that this receptor contributes to an inflammatory switch through its association and disassociation with transcriptional repressors.⁸ The clinical importance of PPARs originates with fibrates and thiazolidinediones (TZDs), which respectively act on PPAR and PPAR and are used to ameliorate hyperlipidemia and hyperglycemia in subjects with type 2 diabetes mellitus (T2DM). Fibrates, such as gemfibrozil, clofibrate, fenofibrate, and bezofibrate, are drugs that effectively reduce triglycerides (TG) and free fatty acids (FFA) and increase high-density lipoproteins-cholesterol.^9–12 Fibrates also improve glucose tolerance in T2DM patients, although this activity might be attributable to the fact that some of these compounds also have potential PPAR activity.¹³ TZDs, such as rosiglitazone, pioglitazone, troglitazone, and ciglitazone, are insulin-sensitizing drugs and have constituted a major advance in the recent therapeutic management of T2DM.^14–16 In addition to . . . [Full Text of this Article]