Control of macrophage activation and function by PPARs.
Abstract: Macrophages, a key component of the innate defense against pathogens, participate in the initiation and resolution of inflammation, and in the maintenance of tissues. These diverse and at times antithetical functions of macrophages are executed via distinct activation states, ranging from classical to alternative to deactivation. Because the dysregulation of macrophage activation is pathogenically linked to various metabolic, inflammatory and immune disorders, regulatory proteins controlling macrophage activation have emerged as important new therapeutic targets. Here, the mechanisms by which peroxisome proliferator-activated receptors (PPARs) transcriptionally regulate macrophage activation in health and disease states, including obesity, insulin resistance and cardiovascular disease, are reviewed.
Division of Endocrinology, Metabolism and Gerontology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305-5103, USA. achawla@stanford.edu
Ajay
A
Chawla
D000818:Animals; D017209:Apoptosis; D002318:Cardiovascular Diseases / Q000503:physiopathology*; D016207:Cytokines / Q000502:physiology; D004195:Disease Models, Animal; D006373:Helminthiasis / Q000503:physiopathology; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D018664:Interleukin-12 / Q000378:metabolism / Q000502:physiology; D008262:Macrophage Activation / Q000502:physiology; D008264:Macrophages / Q000166:cytology / Q000502:physiology*; D009000:Monocytes / Q000166:cytology; D009765:Obesity / Q000503:physiopathology; D047492:Peroxisome Proliferator-Activated Receptors / Q000235:genetics / Q000502:physiology*; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism / Q000502:physiology
D016207:Cytokines; D047492:Peroxisome Proliferator-Activated Receptors; D014409:Tumor Necrosis Factor-alpha; D018664:Interleukin-12