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Peroxisome Proliferator-Activated Receptors and Acute Lung Injury

Peroxisome proliferator-activated receptors are ligand-activated transcription factors belonging to the nuclear hormone receptor superfamily. PPARs regulate several metabolic pathways by binding to sequence-specific PPAR response elements in the promoter region of target genes, including lipid biosy...

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Detalles Bibliográficos
Autores principales: Paola, Rosanna Di, Cuzzocrea, Salvatore
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1940050/
https://www.ncbi.nlm.nih.gov/pubmed/17710233
http://dx.doi.org/10.1155/2007/63745
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author Paola, Rosanna Di
Cuzzocrea, Salvatore
author_facet Paola, Rosanna Di
Cuzzocrea, Salvatore
author_sort Paola, Rosanna Di
collection PubMed
description Peroxisome proliferator-activated receptors are ligand-activated transcription factors belonging to the nuclear hormone receptor superfamily. PPARs regulate several metabolic pathways by binding to sequence-specific PPAR response elements in the promoter region of target genes, including lipid biosynthesis and glucose metabolism. Recently, PPARs and their respective ligands have been implicated as regulators of cellular inflammatory and immune responses. These molecules are thought to exert anti-inflammatory effects by negatively regulating the expression of proinflammatory genes. Several studies have demonstrated that PPAR ligands possess anti-inflammatory properties and that these properties may prove helpful in the treatment of inflammatory diseases of the lung. This review will outline the anti-inflammatory effects of PPARs and PPAR ligands and discuss their potential therapeutic effects in animal models of inflammatory lung disease.
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spelling pubmed-19400502007-08-20 Peroxisome Proliferator-Activated Receptors and Acute Lung Injury Paola, Rosanna Di Cuzzocrea, Salvatore PPAR Res Review Article Peroxisome proliferator-activated receptors are ligand-activated transcription factors belonging to the nuclear hormone receptor superfamily. PPARs regulate several metabolic pathways by binding to sequence-specific PPAR response elements in the promoter region of target genes, including lipid biosynthesis and glucose metabolism. Recently, PPARs and their respective ligands have been implicated as regulators of cellular inflammatory and immune responses. These molecules are thought to exert anti-inflammatory effects by negatively regulating the expression of proinflammatory genes. Several studies have demonstrated that PPAR ligands possess anti-inflammatory properties and that these properties may prove helpful in the treatment of inflammatory diseases of the lung. This review will outline the anti-inflammatory effects of PPARs and PPAR ligands and discuss their potential therapeutic effects in animal models of inflammatory lung disease. Hindawi Publishing Corporation 2007 2007-07-09 /pmc/articles/PMC1940050/ /pubmed/17710233 http://dx.doi.org/10.1155/2007/63745 Text en Copyright © 2007 R. Di Paola and S. Cuzzocrea. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Paola, Rosanna Di
Cuzzocrea, Salvatore
Peroxisome Proliferator-Activated Receptors and Acute Lung Injury
title Peroxisome Proliferator-Activated Receptors and Acute Lung Injury
title_full Peroxisome Proliferator-Activated Receptors and Acute Lung Injury
title_fullStr Peroxisome Proliferator-Activated Receptors and Acute Lung Injury
title_full_unstemmed Peroxisome Proliferator-Activated Receptors and Acute Lung Injury
title_short Peroxisome Proliferator-Activated Receptors and Acute Lung Injury
title_sort peroxisome proliferator-activated receptors and acute lung injury
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1940050/
https://www.ncbi.nlm.nih.gov/pubmed/17710233
http://dx.doi.org/10.1155/2007/63745
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