Growth Signals, Inflammation, and Vascular Perturbations Mechanistic Links Between Obesity, Metabolic Syndrome, and Cancer
Growth Signals, Inflammation, and Vascular Perturbations Mechanistic Links Between Obesity, Metabolic Syndrome, and Cancer
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DOI：
10.1161/atvbaha.111.241927
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发表时间：
2012-08-01
影响因子：
8.7
通讯作者：
Hursting, Marcie J.
中科院分区：
文献类型：
--
作者：
Hursting, Stephen D.;Hursting, Marcie J.
美国近35%的成年人和20%的儿童肥胖，定义为体重指数>= 30 kg/m（2）。肥胖，伴随着代谢失调，通常表现为代谢综合征，是许多癌症的既定危险因素。在肥胖状态的促生长促炎环境中，巨噬细胞、脂肪细胞和上皮细胞之间的相互作用通过肥胖相关激素、细胞因子和其他可能增加癌症风险和进展的介质发生。这篇综述综合了肥胖与癌症联系的关键生物学机制的证据，特别强调了肥胖相关的生长因子信号传导、炎症和血管完整性过程的增强。这些相互关联的途径代表了破坏肥胖-癌症联系的可能机制靶点。（Arterioscler Thromb Vasc Biol.2012;32：1766-1770.）
Nearly 35% of adults and 20% of children in the United States are obese, defined as a body mass index >= 30 kg/m(2). Obesity, which is accompanied by metabolic dysregulation often manifesting in the metabolic syndrome, is an established risk factor for many cancers. Within the growth-promoting, proinflammatory environment of the obese state, cross talk between macrophages, adipocytes, and epithelial cells occurs via obesity-associated hormones, cytokines, and other mediators that may enhance cancer risk and progression. This review synthesizes the evidence on key biological mechanisms underlying the obesity-cancer link, with particular emphasis on obesity-associated enhancements in growth factor signaling, inflammation, and vascular integrity processes. These interrelated pathways represent possible mechanistic targets for disrupting the obesity-cancer link. (Arterioscler Thromb Vasc Biol. 2012;32:1766-1770.)