RAGE-Mediated Inflammation, Type 2 Diabetes, and Diabetic Vascular Complication.
RAGE-Mediated Inflammation, Type 2 Diabetes, and Diabetic Vascular Complication.
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DOI：
10.3389/fendo.2013.00105
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发表时间：
2013
影响因子：
5.2
通讯作者：
Yamamoto H
中科院分区：
文献类型：
--
作者：
Yamamoto Y;Yamamoto H
肥胖与炎症和2型糖尿病有关。由细胞和分子组成的先天免疫系统在炎症反应中起着重要作用。免疫细胞如巨噬细胞及其细胞表面模式识别受体(PRRs)是天然免疫促进炎症反应的代表。晚期糖基化终产物受体(RAGE)是PRRs的成员之一，是一种将危险信号传递给身体的促炎分子装置。在一定条件下，RAGE在脂肪细胞、免疫细胞、内皮细胞和胰腺β细胞中均有表达。据报道，RAGE与脂肪细胞肥大和胰岛素抵抗有关。RAGE介导的肥胖和炎症调节可能与2型糖尿病和糖尿病血管并发症有关。
Obesity is associated with inflammation and type 2 diabetes. Innate immune system comprised of cellular and molecular components plays an important role in the inflammatory reactions. Immune cells like macrophages and their cell surface pattern-recognition receptors (PRRs) are representative for innate immunity promoting inflammatory reactions. The receptor for advanced glycation end-products (RAGE) is a member of PRRs and a proinflammatory molecular device that mediates danger signals to the body. The expression of RAGE is observed in adipocytes as well as immune cells, endothelial cells, and pancreatic β cells under certain conditions. It has been reported that RAGE is implicated in adipocyte hypertrophy and insulin resistance. RAGE-mediated regulation of adiposity and inflammation may attribute to type 2 diabetes and diabetic vascular complications.