The role of endothelial cells in inflamed adipose tissue.

Coralie Sengenès 1 Alexandra Miranville 2 Karine Lolmède 1 Cyrile Anne Curat 2 Anne Bouloumié 1, *
* Auteur correspondant
1 Unité de recherche sur les obésités
2 Institute of Cardiovascular Physiology
Abstract : In recent years, the general concept has emerged that chronic low-grade inflammation can be the condition linking excessive development of adipose tissue (AT) and obesity-associated pathologies such as type II diabetes and atherosclerosis. Moreover, the evidence that the growth of the fat mass was associated with an accumulation of adipose tissue macrophages (ATM) has raised the hypothesis that the development of an inflammatory process within the growing fat mass is a primary event involved in the genesis of systemic metabolic and vascular alterations. As ATM originate from the bone marrow/blood compartment, enhanced macrophage recruitment to growing AT is suspected. However, the mechanisms responsible for attracting the blood cells and their entry into the fat mass remain to be clearly defined. The present review highlights the key role of endothelial cells in the control of the inflammatory process and describes the potential involvement of AT-endothelial cells as well as the factors involved in the regulation of their phenotype in the 'inflamed fat tissue'.
Type de document :
Article dans une revue
Journal of Internal Medicine, Wiley, 2007, 262 (4), pp.415-21. 〈10.1111/j.1365-2796.2007.01853.x〉
Liste complète des métadonnées
http://www.hal.inserm.fr/inserm-00409797
Contributeur : Marie Francoise Simon <>
Soumis le : jeudi 13 août 2009 - 08:40:07
Dernière modification le : vendredi 16 novembre 2018 - 17:34:18

Lien texte intégral

openaccess

Identifiants

Collections

UNIV-TLSE3

Citation

Coralie Sengenès, Alexandra Miranville, Karine Lolmède, Cyrile Anne Curat, Anne Bouloumié. The role of endothelial cells in inflamed adipose tissue.. Journal of Internal Medicine, Wiley, 2007, 262 (4), pp.415-21. 〈10.1111/j.1365-2796.2007.01853.x〉. 〈inserm-00409797〉

Exporter

BibTeX TEI DC DCterms EndNote

Partager

Métriques

Consultations de la notice

192

Contact

support.ccsd.cnrs.fr
hal.support@ccsd.cnrs.fr
Logo CCSD