Metabolic Regulation of Adipose Tissue Macrophage Function in Obesity and Diabetes.

Metabolic Regulation of Adipose Tissue Macrophage Function in Obesity and Diabetes.
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肥胖与糖尿病中脂肪组织巨噬细胞功能的代谢调控

DOI:
10.1089/ars.2017.7060
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发表时间:
2018-07-20
影响因子:
6.6
通讯作者:
McNeill E
McNeill E
中科院分区:
生物学2区
文献类型:
--
作者:
Appari M;Channon KM;McNeill E

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重要性:肥胖和糖尿病与炎症通路的慢性激活相关,炎症通路是胰岛素抵抗(IR)、2型糖尿病(T2 D)和心血管疾病发病机制之间的重要机制联系。这些代谢性疾病的发展与脂肪组织巨噬细胞(ATM)的数量和表型的变化有关。新出现的证据表明,ATM释放促炎细胞因子,类似于经典活化的M1巨噬细胞,直接导致IR或T2 D。相比之下,来自瘦健康个体的脂肪组织(AT)含有具有较少炎性M2表型的巨噬细胞。最新进展:最近的研究表明,巨噬细胞表型与巨噬细胞代谢的深刻变化有关。关键问题:本文综述了巨噬细胞在AT炎症和肥胖中的作用,以及巨噬细胞功能的代谢变化,这些变化与激活有关,这些变化支持了巨噬细胞在IR和T2 D发病机制中的作用。我们强调了当前从代谢疾病和AT生物学领域以及更广泛的炎症生物学领域改变巨噬细胞代谢的靶点。未来发展方向:随着我们对AT中巨噬细胞代谢编程的了解的建立,靶向巨噬细胞生物学的这一方面作为代谢性疾病的治疗策略的范围将越来越大。抗氧化剂。氧化还原信号。29,297-312.
Significance: Obesity and diabetes are associated with chronic activation of inflammatory pathways that are important mechanistic links between insulin resistance (IR), type 2 diabetes (T2D), and cardiovascular disease pathogenesis. The development of these metabolic diseases is associated with changes in both the number and phenotype of adipose tissue macrophages (ATMs). Emerging lines of evidence have shown that ATMs release proinflammatory cytokines similar to classically activated M1 macrophages, which directly contribute to IR or T2D. In contrast, adipose tissue (AT) from lean healthy individuals contains macrophages with a less inflammatory M2 phenotype. Recent Advances: Recent research has shown that macrophage phenotype is linked to profound changes in macrophage cellular metabolism. Critical Issues: This review focuses on the role of macrophages in AT inflammation and obesity, and the metabolic changes in macrophage function that occur with activation that underpin their role in the pathogenesis of IR and T2D. We highlight current targets for altering macrophage metabolism from both within the field of metabolic disease and AT biology and more widely within inflammatory biology. Future Directions: As our knowledge of macrophage metabolic programming in AT builds, there will be increasing scope for targeting this aspect of macrophage biology as a therapeutic strategy in metabolic diseases. Antioxid. Redox Signal. 29, 297–312.
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