Macrophage metabolic reprogramming during chronic lung disease.

Macrophage metabolic reprogramming during chronic lung disease.
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慢性肺部疾病中的巨噬细胞代谢重编程。

DOI:
10.1038/s41385-020-00356-5
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发表时间:
2021-03
期刊:
影响因子:
8
通讯作者:
Byrne AJ
Byrne AJ
中科院分区:
医学1区
文献类型:
--
作者:
Ogger PP;Byrne AJ

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气道巨噬细胞(AM)在维持肺免疫耐受中起关键作用。组织定制,高度专业化和战略定位,AM是肺内稳态的关键哨兵。在过去的十年中,我们对代谢如何成为关键巨噬细胞功能的基础的理解发生了革命。虽然这些最初的观察是在稳态或使用体外极化巨噬细胞进行的,但最近的研究表明,在许多慢性肺部疾病(CLD)期间,AM会调整其代谢特征以适应其局部生态位。通过产生活性氧(ROS)用于病原体防御,利用有氧糖酵解快速产生细胞因子,并利用线粒体呼吸来刺激炎症反应,AM利用代谢重编程用于宿主防御,尽管这些变化也可能支持慢性病理学。 本文综述了CLDs过程中AM表型和功能的代谢改变。特别强调的是如何我们的新的理解AM代谢可塑性可能被利用开发AM为重点的治疗。
Airway macrophages (AMs) play key roles in the maintenance of lung immune tolerance. Tissue tailored, highly specialised and strategically positioned, AMs are critical sentinels of lung homoeostasis. In the last decade, there has been a revolution in our understanding of how metabolism underlies key macrophage functions. While these initial observations were made during steady state or using in vitro polarised macrophages, recent studies have indicated that during many chronic lung diseases (CLDs), AMs adapt their metabolic profile to fit their local niche. By generating reactive oxygen species (ROS) for pathogen defence, utilising aerobic glycolysis to rapidly generate cytokines, and employing mitochondrial respiration to fuel inflammatory responses, AMs utilise metabolic reprogramming for host defence, although these changes may also support chronic pathology. This review focuses on how metabolic alterations underlie AM phenotype and function during CLDs. Particular emphasis is given to how our new understanding of AM metabolic plasticity may be exploited to develop AM-focused therapies.
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