Department of Pediatrics and Communicable Diseases, and Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Sci Transl Med. 2010 Feb 24;2(20):20ps7. doi: 10.1126/scitranslmed.3000850.
A body of research has strongly implicated inflammation in the genesis of obesity-associated diseases such as type 2 diabetes and cardiovascular disease. An outstanding issue is how obesity-induced metabolic signals are translated into an inflammatory response. In this issue of Science Translational Medicine, Kishore et al. demonstrate that the action of free fatty acids on adipose tissue macrophages dynamically regulates the expression of plasminogen activator inhibitor-1, a serine protease inhibitor that suppresses the breakdown of blood clots. Their data suggest that these macrophages sit in a specialized microenvironment that senses metabolic signals from fat cells and the circulation and integrates them to produce an inflammatory signal.
大量研究强烈表明炎症与肥胖相关疾病(如 2 型糖尿病和心血管疾病)的发生有关。一个悬而未决的问题是肥胖引起的代谢信号如何转化为炎症反应。在本期《科学转化医学》中,Kishore 等人证明,游离脂肪酸对脂肪组织巨噬细胞的作用可以动态调节纤溶酶原激活物抑制剂-1 的表达,纤溶酶原激活物抑制剂-1 是一种丝氨酸蛋白酶抑制剂,可抑制血栓的分解。他们的数据表明,这些巨噬细胞位于一个特殊的微环境中,可以感知来自脂肪细胞和循环系统的代谢信号,并将其整合以产生炎症信号。