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Usage Information

HIF1α and metabolic reprogramming in inflammation
Sarah E. Corcoran, Luke A.J. O’Neill
Sarah E. Corcoran, Luke A.J. O’Neill
Published August 29, 2016
Citation Information: J Clin Invest. 2016;126(10):3699-3707. https://doi.org/10.1172/JCI84431.
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HIF1α and metabolic reprogramming in inflammation

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Abstract

HIF1α is a common component of pathways involved in the control of cellular metabolism and has a role in regulating immune cell effector functions. Additionally, HIF1α is critical for the maturation of dendritic cells and for the activation of T cells. HIF1α is induced in LPS-activated macrophages, where it is critically involved in glycolysis and the induction of proinflammatory genes, notably Il1b. The mechanism of LPS-stimulated HIF1α induction involves succinate, which inhibits prolyl hydroxylases (PHDs). Pyruvate kinase M2 (PKM2) is also induced and interacts with and promotes the function of HIF1α. In another critical inflammatory cell type, Th17 cells, HIF1α acts via the retinoic acid–related orphan receptor-γt (RORγt) to drive Th17 differentiation. HIF1α is therefore a key reprogrammer of metabolism in inflammatory cells that promotes inflammatory gene expression.

Authors

Sarah E. Corcoran, Luke A.J. O’Neill

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Usage data is cumulative from June 2024 through June 2025.

Usage JCI PMC
Text version 3,791 1,777
PDF 335 347
Figure 322 9
Table 102 0
Citation downloads 101 0
Totals 4,651 2,133
Total Views 6,784
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Usage information is collected from two different sources: this site (JCI) and Pubmed Central (PMC). JCI information (compiled daily) shows human readership based on methods we employ to screen out robotic usage. PMC information (aggregated monthly) is also similarly screened of robotic usage.

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