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Iron overloaded polarizes macrophage to proinflammation phenotype through ROS/acetyl‐p53 pathway

机译:铁超载通过ROS /乙酰p53途径使巨噬细胞极化为促炎表型

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摘要

PurposeMacrophages play critical roles in inflammation and wound healing and can be divided into two subtypes: classically activated (M1) and alternatively activated (M2) macrophages. Macrophages also play important roles in regulating iron homeostasis, and intracellular iron accumulation induces M1‐type macrophage polarization which provides a potential approach to tumor immunotherapy through M2 tumor‐associated macrophage repolarization. However, the mechanisms underlying iron‐induced M1 polarization remain unclear.
机译:目的巨噬细胞在炎症和伤口愈合中起关键作用,可分为两种亚型:经典激活(M1)和交替激活(M2)巨噬细胞。巨噬细胞在调节铁稳态中也起着重要作用,并且细胞内铁的积累会诱导M1型巨噬细胞极化,这为通过M2肿瘤相关巨噬细胞复极化提供了一种潜在的肿瘤免疫治疗方法。但是,铁诱导的M1极化的潜在机制仍不清楚。

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