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首页> 外文期刊>Cell metabolism >Efferocytosis Fuels Requirements of Fatty Acid Oxidation and the Electron Transport Chain to Polarize Macrophages for Tissue Repair
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Efferocytosis Fuels Requirements of Fatty Acid Oxidation and the Electron Transport Chain to Polarize Macrophages for Tissue Repair

机译：癫痫症燃料燃料氧化要求和电子传输链偏振巨噬细胞组织修复

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During wound injury, efferocytosis fills the macrophage with a metabolite load nearly equal to the phagocyte itself. A timely question pertains to how metabolic phagocytic signaling regulates the signature anti-inflammatory macrophage response. Here we report the metabolome of activated macrophages during efferocytosis to reveal an interleukin-10 (IL-10) cytokine escalation that was independent of glycolysis yet bolstered by apoptotic cell fatty acids and mitochondrial beta-oxidation, the electron transport chain, and heightened coenzyme NAD(+). Loss of IL-10 due to mitochondrial complex III defects was remarkably rescued by adding NAD(+) precursors. This activated a SIRTUIN1 signaling cascade, largely independent of ATP, that culminated in activation of IL-10 transcription factor PBX1. II-10 activation by the respiratory chain was also important in vivo, as efferocyte mitochondrial dysfunction led to cardiac rupture after myocardial injury. These findings highlight a new paradigm whereby macrophages leverage efferocytic metabolites and electron transport for anti-inflammatory reprogramming that culminates in organ repair.
机译：在伤口损伤期间，癫痫细胞菌填充巨噬细胞，其代谢物负荷几乎等于吞噬细胞本身。及时的问题涉及代谢吞噬信号传导如何调节特征抗炎巨噬细胞反应。在这里，我们在癫痫细胞瘤期间报告了活化巨噬细胞的代谢物，揭示白细胞介素-10（IL-10）细胞因子升级，其独立于糖醇分解，尤其凋亡细胞脂肪酸和线粒体β-氧化，电子传输链和加强辅酶NAD。 （+）。通过添加NAD（+）前体显着抵押由于线粒体复合物III缺陷引起的IL-10的损失。这激活了Sirtuin1信号传导级联，主要独立于ATP，其在IL-10转录因子PBX1的激活中终止。 II-10通过呼吸链激活在体内也很重要，因为活细胞线粒体功能障碍导致心肌损伤后心脏破裂。这些发现突出了一种新的范式，即巨噬细胞利用患有效力性代谢物和电子传输用于抗炎重编程，以促使器官修复。

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