Hypoxia and the regulation of myeloid cell metabolic imprinting: consequences for the inflammatory response

被引:65
作者
Sadiku, Pranvera [1 ]
Walmsley, Sarah R. [1 ]
机构
[1] Univ Edinburgh, Ctr Inflammat Res, Queens Med Res Inst, Edinburgh, Midlothian, Scotland
基金
英国惠康基金;
关键词
hypoxia-inducible factors; hypoxia; immunometabolism; macrophages; neutrophils; NITRIC-OXIDE PRODUCTION; FATTY-ACIDS; HIF-ALPHA; MACROPHAGE POLARIZATION; NEUTROPHIL SURVIVAL; INDUCIBLE FACTORS; KETONE-BODIES; ATP RELEASE; OXYGEN; ACTIVATION;
D O I
10.15252/embr.201847388
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Inflamed and infected tissue sites are characterised by oxygen and nutrient deprivation. The cellular adaptations to insufficient oxygenation, hypoxia, are mainly regulated by a family of transcription factors known as hypoxia-inducible factors (HIFs). The protein members of the HIF signalling pathway are critical regulators of both the innate and adaptive immune responses, and there is an increasing body of evidence to suggest that the elicited changes occur through cellular metabolic reprogramming. Here, we review the literature on innate immunometabolism to dateand discuss the role of hypoxia in innate cell metabolic reprogramming, and how this determines immune responses.
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页数:11
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