SOCS, inflammation, and metabolism
SOCS, inflammation, and metabolism
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发表时间：
2014-10
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通讯作者：
K. Inagaki-Ohara;A. Yoshimura
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作者：
K. Inagaki-Ohara;A. Yoshimura
肥胖的特点是发生低度慢性炎症，这是能量代谢缺陷的一个促成因素。肥胖是代谢失调的标志，是一种生活方式疾病，会导致糖尿病、高血压和血脂异常。此外，最近的研究警告说，肥胖可能是某些癌症的危险因素，并会加剧传染病。这种关联被称为“代谢多米诺骨牌”。细胞因子信号传导抑制蛋白 (SOCS) 是 JAK-STAT 信号通路介导的细胞因子和激素信号传导的负反馈调节剂。 SOCS 蛋白通过 JAK-STAT 依赖性细胞因子和 Toll 样受体 (TLR) 信号传导来调节细胞间通讯，并且它们可能受到脂肪酸和葡萄糖等饮食因素的影响。在这篇综述中，我们重点关注 JAK-STAT-SOCS 信号级联在代谢紊乱和肥胖相关疾病中的作用。
Obesity is characterized by the development of low-grade chronic inflammation, which is a contributing factor in defective energy metabolism. A hallmark of metabolic dysregulation, obesity is a life-style disease that contributes to diabetes, hypertension, and dyslipidemia. Further, recent studies warn that obesity can be a risk factor for certain cancers and exacerbates infectious diseases. This association is called the “metabolic domino”. Suppressor of cytokine signaling (SOCS) proteins are negative feedback regulators of cytokine and hormone signaling mediated by the JAK-STAT signaling pathway. SOCS proteins regulate cell-cell communication through JAK-STAT-dependent cytokines and signaling by Toll-like receptors (TLRs) and they may be influenced by dietary factors such as fatty acids and glucose. In this review, we focus on the role of the JAK-STAT-SOCS signaling cascade in metabolic disorder and obesity-related diseases.