巨噬细胞极化
免疫系统
炎症
安普克
β氧化
巨噬细胞
脂肪酸
脂肪酸代谢
过氧化物酶体
生物
过氧化物酶体增殖物激活受体
脂肪细胞蛋白2
新陈代谢
细胞生物学
生物化学
受体
蛋白激酶A
激酶
免疫学
体外
作者
Dmitry Namgaladze,Bernhard Brüne
标识
DOI:10.1016/j.bbalip.2016.09.002
摘要
Recent research considerably changed our knowledge how cellular metabolism affects the immune system. We appreciate that metabolism not only provides energy to immune cells, but also actively influences diverse immune cell phenotypes. Fatty acid metabolism, particularly mitochondrial fatty acid oxidation (FAO) emerges as an important regulator of innate and adaptive immunity. Catabolism of fatty acids also modulates the progression of disease, such as the development of obesity-driven insulin resistance and type II diabetes. Here, we summarize (i) recent developments in research how FAO modulates inflammatory signatures in macrophages in response to saturated fatty acids, and (ii) the role of FAO in regulating anti-inflammatory macrophage polarization. In addition, we define the contribution of AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptors (PPARs), in controlling macrophage biology towards fatty acid metabolism and inflammation.
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