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Review
. 2010 Feb;55(2):437-44.
doi: 10.1161/HYPERTENSIONAHA.109.144170. Epub 2009 Dec 28.

Endothelial and vascular muscle PPARgamma in arterial pressure regulation: lessons from genetic interference and deficiency

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Review

Endothelial and vascular muscle PPARgamma in arterial pressure regulation: lessons from genetic interference and deficiency

Curt D Sigmund. Hypertension. 2010 Feb.
No abstract available

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Figures

Figure 1
Figure 1. Schematic Representation of the PPARγ Transcriptional Mechanism
A. Transcriptional repression by unliganded PPARγ. B. Transcriptional induction in the presence of ligand. C. Diminished transcription due to the presence of dominant negative PPARγ. D. Intermediate transcription in PPARγ-deficiency. The length and width of the arrows reflect levels of transcription. PPARγ is orange and RXR is blue. CoR, co-repressor; HDAC, histone deacetylase; CoA, co-activator; PGC1α, PPARγ coactivator-1 alpha; SRC, steroid receptor coactivator; RNAP, RNA polymerase; TFs, transcription factors; PPRE, PPARγ response element.
Figure 2
Figure 2. Model of PPARγ Effects in Endothelium and Vascular Muscle
Schematic model showing some of the main effects of PPARγ in endothelium (EC) and vascular muscle (SMC). A. In the presence of PPARγ, ligand mediated activation will provide anti-inflammatory, and anti-oxidant protection, promote vasodilation and inhibit contractile actions of agonists. B. The absence of PPARγ promotes endothelial dysfunction in response to high fat diet, decrease NO-mediated vasodilation, and markedly augmented contractile response to ET-1, and hypertension.

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