Titre du document / Document title

PPARγ activity in the vessel wall : Anti-atherogenic properties

Auteur(s) / Author(s)

REISS Allison B. ⁽¹⁾ ; VAGELL Michael E. ⁽¹⁾ ;

Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)

⁽¹⁾ Vascular Biology Institute, Department of Medicine, Winthrop- University Hospital, 222 Station Plaza North, Mineola, NY 11501, ETATS-UNIS

Résumé / Abstract

The nuclear receptor peroxisome proliferator-activated receptor y (PPARy) is a ligand-dependent transcription factor that controls the expression of specific target genes involved in adipogenesis, inflammatory responses, and lipid metabolism. Atherosclerotic plaque progression is influenced by intraplaque inflammation and extracellular matrix deposition. Anti-inflammatory, anti-proliferative and anti-protease activity of PPARγ may modulate the atherosclerotic process. PPARy is expressed in atherosclerotic lesions of human coronary arteries and has direct anti-inflammatory effects in the vascular wall. Thiazolidinediones (TZD) are ligands for PPARy used therapeutically to enhance insulin-mediated glucose uptake in persons with type 2 diabetes. These agents may also exert anti-atherogenic effects on cells of the vessel wall including macrophages. vascular endothelium and vascular smooth muscle. This review discusses the impact of PPARy and its activators in the numerous processes involved in the formation of atherosclerotic lesions. We provide an overview of in vitro and in vivo data in cell lines, animal models, and humans demonstrating the ways in which PPARy activation alters the biology of the arterial wall.

Revue / Journal Title

Current medicinal chemistry   ISSN 0929-8673 

Source / Source

2006, vol. 13, n^o26, pp. 3227-3238 [12 page(s) (article)] (158 ref.)

Langue / Language

Anglais

Editeur / Publisher

Bentham Science, Oak Park, IL, ETATS-UNIS  (1994) (Revue)

Mots-clés anglais / English Keywords

Vascular disease ; Cardiovascular disease ; Thiazolidinedione derivatives ; Enzyme ; Oxidoreductases ; Liver X receptor ; Signal transduction ; Hormonal receptor ; Biological receptor ; Degradation product ; Cholesterol ; Steroid ; Nuclear receptor ; Review ; 27-Hydroxycholesterol 7-α-monooxygenase ; Atherosclerosis ; Prevention ; Atheroma ; ABC transporter ; Pioglitazone ; Rosiglitazone ; Vascular wall ; Biological activity ; PPAR-γ receptor ;

Mots-clés français / French Keywords

Vaisseau sanguin pathologie ; Appareil circulatoire pathologie ; Thiazolidinedione dérivé ; Enzyme ; Oxidoreductases ; Récepteur LXR ; Thiazolidine dérivé ; Prostaglandine D2 analogue ; Oxystérol ; Transduction signal ; Récepteur hormonal ; Récepteur biologique ; Produit dégradation ; Cholestérol ; Stéroïde ; Récepteur nucléaire ; Article synthèse ; 27-Hydroxycholesterol 7-α-monooxygenase ; Athérosclérose ; Prévention ; Athérome ; Transporteur ABC ; Pioglitazone ; Rosiglitazone ; Paroi vasculaire ; Activité biologique ; Récepteur PPAR-γ ;

Mots-clés espagnols / Spanish Keywords

Vaso sanguíneo patología ; Aparato circulatorio patología ; Tiazolidinediona derivado ; Enzima ; Oxidoreductases ; Transducción señal ; Receptor hormonal ; Receptor biológico ; Producto degradación ; Colesterol ; Esteroide ; Receptor nuclear ; Artículo síntesis ; 27-Hydroxycholesterol 7-α-monooxygenase ; Ateroesclerosis ; Prevención ; Ateroma ; Transportador ABC ; Pioglitazona ; Rosiglitazona ; Pared vascular ; Actividad biológica ; Receptor PPAR-γ ;

Mots-clés d'auteur / Author Keywords

27-hydroxylase ; oxysterol ; rosiglitazone ; pioglitazone ; atheroma ; LXR ; 15d-PGJ2 ; ABCA1 ;

Localisation / Location

INIST-CNRS, Cote INIST : 22999, 35400014298203.0100