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(Hypertension. 2007;50:847.)
© 2007 American Heart Association, Inc.

Editorial Commentaries

Peroxisome Proliferator-Activated Receptor–

Friend or Foe?

Chana Yagil; Yoram Yagil

From the Laboratory for Molecular Medicine, Faculty of Health Sciences, Ben-Gurion University, Ashkelon, Israel.

Correspondence to Chana Yagil, Laboratory for Molecular Medicine, Faculty of Health Sciences, Ben-Gurion University, Barzilai Medical Center Campus, Ashkelon 78306, Israel. E-mail: chyagil@bgu.ac.il

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

The quest for better understanding for the pathophysiological basis of hypertension and atherosclerosis is ongoing. The complexity of hypertension and atherosclerosis and of the underlying mechanisms is becoming increasingly apparent. The number of candidate genes and molecular pathways that are involved is increasing in parallel. In the present issue of Hypertension, Tordjman et al¹ explore the role of the candidate gene, peroxisome proliferator-activated receptor (PPAR)– (reviewed extensively and comprehensively in the Web site dedicated to PPAR: http://ppar.cas.psu.edu/), in the regulation of blood pressure and atherogenesis. The investigators follow up their previous observation that PPAR-deficient mice were protected from hypertension and atherosclerosis.² They currently report that, in a mouse experimental model of high renin and elevated angiotensin II levels in which the PPAR gene has been knocked out, hypertension and diet-induced atherosclerosis are averted.

PPAR is widely distributed in the vasculature, as well as in other tissues and organs. PPAR is a nuclear receptor, one in a family of at least 3 transcription factors that have been connected to cell metabolism and differentiation. The peroxisome, an intracellular organelle that is capable of self-replicating, is present in all eukaryotic cells that contain enzymes, some of which are oxidative enzymes. The effects of PPAR that we are currently dealing with, affecting blood pressure and atherogenesis, however, are thought not to be related to peroxisome proliferation or activation but rather to other intracellular pathways, some of which have been elucidated, whereas others remain to be clarified.³ PPAR has pleiotropic effects and controls . . . [Full Text of this Article]

Related Article:

Absence of Peroxisome Proliferator-Activated Receptor- Abolishes Hypertension and Attenuates Atherosclerosis in the Tsukuba Hypertensive Mouse

Karen M. Tordjman, Clay F. Semenkovich, Trey Coleman, Rachel Yudovich, Stella Bak, Etty Osher, Michal Vechoropoulos, and Naftali Stern
Hypertension 2007 50: 945-951. [Abstract] [Full Text] [PDF]