%0 Journal Article %T PPARbeta in macrophages and atherosclerosis %+ Institut de Recherche sur le Cancer et le Vieillissement (IRCAN) %+ Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 (RNMCD) %A Chinetti-Gbaguidi, Giulia %A Staels, Bart %Z Fondation de France; Fondation pour la Recherche Médicale (DPC2011122981); European Commission %< avec comité de lecture %@ 0300-9084 %J Biochimie %I Elsevier %8 2017 %D 2017 %R 10.1016/j.biochi.2016.12.008 %M 28011212 %K Atherosclerotic lesion %K Gene regulation %K Inflammation %K Lipid metabolism %K Transcription factor %Z Life Sciences [q-bio]/Biochemistry, Molecular BiologyJournal articles %X Macrophages are central cells in the genesis and development of atherosclerosis, one of themajor causes of cardiovascular diseases. Macrophages take up lipids (mainly cholesterol andtriglycerides) from lipoproteins thus transforming into foam cells. Moreover, through theefflux pathway, macrophages are the main actors of the elimination of excessive tissuecholesterol toward extra-cellular acceptors. Macrophages participate in the control ofinflammation by displaying different functional phenotypes, from the M1 pro-inflammatoryto the M2 anti-inflammatory state.The nuclear receptor Peroxisome Proliferator-Activated Receptor (PPAR)beta (also calledPPARdelta or PPARbeta/delta) is expressed in macrophages where it plays a different role in the controlof lipid metabolism, inflammation and phagocytosis of apoptotic cells.This review will summarize our current understanding of how PPARbeta regulates macrophagebiology and its impact on atherosclerosis. Differences between studies and species-specificmacrophage gene regulation will be discussed. %G English %2 https://inserm.hal.science/inserm-01433144/document %2 https://inserm.hal.science/inserm-01433144/file/Chinetti%20R1.pdf %L inserm-01433144 %U https://inserm.hal.science/inserm-01433144 %~ INSERM %~ UNICE %~ RIIP %~ CNRS %~ RIIP_LILLE %~ UNIV-COTEDAZUR %~ UNIV-LILLE %~ TEST-HALCNRS %~ RNMCD %~ ANR %~ IRCAN %~ FRM