Lipid chaperones and metabolic inflammation.
Lipid chaperones and metabolic inflammation.
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DOI：
10.4061/2011/642612
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发表时间：
2011
影响因子：
2
通讯作者：
Miura T
中科院分区：
文献类型：
--
作者：
Furuhashi M;Ishimura S;Ota H;Miura T
在过去的十年中，大量证据表明代谢和免疫反应途径的整合。现在已经清楚，肥胖和胰岛素抵抗和 2 型糖尿病等相关疾病与代谢驱动的低度慢性炎症状态（称为“代谢炎症”）有关。几种炎症细胞因子以及脂质和代谢应激途径可以激活代谢炎症，其目标是代谢关键器官和组织，包括脂肪细胞和巨噬细胞，对全身稳态产生不利影响。另一方面，在细胞内部，脂肪酸结合蛋白（FABP）、脂质伴侣家族、内质网（ER）应激和源自线粒体的活性氧在促进代谢引发的炎症中发挥着重要作用。在这里，我们讨论 FABP（尤其是 FABP4 和 FABP5）在代谢炎症和相关疾病（包括肥胖、糖尿病和动脉粥样硬化）中作用的分子和细胞基础。
Over the past decade, a large body of evidence has emerged demonstrating an integration of metabolic and immune response pathways. It is now clear that obesity and associated disorders such as insulin resistance and type 2 diabetes are associated with a metabolically driven, low-grade, chronic inflammatory state, referred to as “metaflammation.” Several inflammatory cytokines as well as lipids and metabolic stress pathways can activate metaflammation, which targets metabolically critical organs and tissues including adipocytes and macrophages to adversely affect systemic homeostasis. On the other hand, inside the cell, fatty acid-binding proteins (FABPs), a family of lipid chaperones, as well as endoplasmic reticulum (ER) stress, and reactive oxygen species derived from mitochondria play significant roles in promotion of metabolically triggered inflammation. Here, we discuss the molecular and cellular basis of the roles of FABPs, especially FABP4 and FABP5, in metaflammation and related diseases including obesity, diabetes, and atherosclerosis.