Evidence map›Paper›PMID 27571407›Full record

ReviewThe Journal of clinical investigation2016

HIF1α and metabolic reprogramming in inflammation.

Sarah E Corcoran, Luke A J O'Neill

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 476 papers.

0numbers the graph read from it
0cells of the map it votes in
476citing papers in PubMed
12.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

476 citing papers in PubMed, 703 citations in OpenAlex.

  1. Dismantling the eDNA-mediated HBioactive materials · 2027
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  13. PKM2: A gatekeeper in macrophage metabolic reprogramming.Journal of pharmaceutical analysis · 2026
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416 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Sarah E Corcoran
Luke A J O'Neill

Funding

Wellcome Trust 109443/Z/15/Z
6 · The paper itself

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.

Indexed as

AnimalsHumansHypoxia-Inducible Factor 1, alpha SubunitInflammationLipopolysaccharidesLymphocytesMetabolic Networks and PathwaysNeutrophilsTranscriptional ActivationHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitLipopolysaccharides

Identifiers

PMID27571407
PMCPMC5096812
OpenAlexW2510362766

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.