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Expressed in all of the cellular elements of the vascular wall, and present in the atherosclerotic plaque, the precise part in the peroxisome proliferator-activated receptor alpha (PPAR) in atherogenesis continues to be controversial. Its recognized impact on lipoprotein metabolism, and largely surrogate endpoints derived from animal studies, helped shape the view that its activation confers protection against atherosclerosis (for evaluation [1]). Huge clinical trials made to assess the potential of fibrates to decrease the price of cardiovascular endpoints have, even so, reached mixed final results, suggesting that benefit may very well be restricted to subsets of subjects with defined lipoprotein abnormalities [2]. We previously reported that ApoE-null mice lacking PPAR were resistant to dietinduced atherosclerosis, despite exhibiting the worsened lipid profile anticipated from the absence of PPAR. Furthermore, the double knockout mice had also a somewhat decrease blood pressure [5]. Though by itself this reduction couldn’t explainthe protection from atherosclerosis, it suggested that PPAR could impact a program central to both atherogenesis and blood pressure regulation. Within this respect, a natural candidate is the renin-angiotensin program (RAS). We subsequently showed that ablation of PPAR totally abolished hypertension and drastically NPY Y4 receptor manufacturer decreased diet-induced atherosclerosis within the Tsukuba hypertensive mouse, a model of angiotensin II (AII-) mediated hypertension and atherosclerosis as a consequence of the transgenic expression in the human renin and angiotensinogen genes. In th.