Abstract
Hypoxia is a hallmark of inflamed, infected or damaged tissue, and the adaptation to inadequate tissue oxygenation is regulated by hypoxia-inducible factors (HIFs). HIFs are key mediators of the cellular response to hypoxia, but they are also associated with pathological stress such as inflammation, bacteriological infection or cancer. In addition, HIFs are central regulators of many innate and adaptive immunological functions, including migration, antigen presentation, production of cytokines and antimicrobial peptides, phagocytosis as well as cellular metabolic reprogramming. A characteristic feature of immune cells is their ability to infiltrate and operate in tissues with low level of nutrients and oxygen. The objective of this article is to discuss the role of HIFs in the function of innate and adaptive immune cells in hypoxia, with a focus on how hypoxia modulates immunometabolism.
Highlights
Institut National de la Santé et de la Recherche Médicale (INSERM), Paris Cardiovascular Research Center, Unit 970, 56 Rue Leblanc, 75015 Paris, France
hypoxia-inducible factors (HIFs) expression can be generated by hypoxia itself, and by others circumstances associated with pathological stress including cancer, inflammation, and bacteriological infection
HIFα subunit is translocated to the nucleus, where response elements (HRE) within target genes, involved in a large type of processes, as cellular formed a complex with HIF-1β, recruit coactivator p300/CBP, and upon binding to the consensus metabolism, proliferation, differentiation, cell survival, migration, apoptosis or angiogenesis
Summary
The oxygen concentration is closely associated with cellular proliferation, division and survival, and is generally maintained by homeostatic mechanisms operating at the cellular and systemic organ (tissue) levels [1,2,3,4,5,6]. HIFα subunit is translocated to the nucleus, where response elements (HRE) within target genes, involved in a large type of processes, as cellular formed a complex with HIF-1β, recruit coactivator p300/CBP, and upon binding to the consensus metabolism, proliferation, differentiation, cell survival, migration, apoptosis or angiogenesis. Hypoxia response elements (HRE) within target genes, involved in a large type of processes, as cellular metabolism, proliferation, differentiation, celldrops, survival, migration, apoptosis or angiogenesis. During hypoxia, when the oxygen level drops, PHDs and FIH become inactive, resulting in HIF-α that control a large number of processes, including cellular metabolism, proliferation, differentiation, stabilization. The HIFα subunit translocates to the nucleus, forms a complex with cell survival, migration, apoptosis or angiogenesis (as shown in Figure 1) [3,8,23,24].
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