Charo Israel F
Gladstone Institute of Cardiovascular Disease, Cardiovascular Research Institute, and Department of Medicine, University of California, San Francisco, San Francisco, CA 94158, USA.
Cell Metab. 2007 Aug;6(2):96-8. doi: 10.1016/j.cmet.2007.07.006.
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.
巨噬细胞协调炎症反应，这在饮食诱导的肥胖中会导致葡萄糖不耐受，在动脉粥样硬化中会导致斑块不稳定。在这群异质性细胞中，存在促炎性（M1）巨噬细胞和抗炎性（M2）巨噬细胞。最近的研究已确定核激素受体PPARγ是在体外和脂肪组织中决定巨噬细胞表型的关键信号分子。在本期《细胞代谢》中，布勒尔等人（2007年）将这一范例扩展到血管壁，他们发现M1和M2巨噬细胞都存在于动脉粥样硬化病变中，并且PPARγ的激活会使循环血液中的单核细胞极化成为M2巨噬细胞。
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