Macrophage polarization and insulin resistance: PPARgamma in control.
Macrophages orchestrate an inflammatory response that contributes to glucose intolerance in diet-induced obesity and plaque instability in atherosclerosis. Within this heterogeneous group of cells are proinflammatory (M1) and anti-inflammatory (M2) macrophages. Recent work has identified the nuclear hormone receptor PPARgamma as a critical signaling molecule in determining macrophage phenotype in vitro and in adipose tissue. In the current issue of Cell Metabolism, Bouhlel et al. (2007) extend this paradigm to the vessel wall by showing that both M1 and M2 macrophages are present in atherosclerotic lesions and that activation of PPARgamma polarizes circulating blood monocytes to become M2 macrophages.
Charo
Israel F
IF
Gladstone Institute of Cardiovascular Disease, Cardiovascular Research Institute, and Department of Medicine, University of California, San Francisco, San Francisco, CA 94158, USA. icharo@gladstone.ucsf.edu
D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D002340:Carotid Artery Diseases / Q000473:pathology; D016764:Cell Polarity; D006801:Humans; D007333:Insulin Resistance; D008264:Macrophages / Q000166:cytology*; D051379:Mice; D009000:Monocytes / Q000166:cytology / Q000187:drug effects; D047495:PPAR gamma / Q000819:agonists / Q000378:metabolism*; D045162:Thiazolidinediones / Q000494:pharmacology
D015415:Biomarkers; D047495:PPAR gamma; D045162:Thiazolidinediones