Evidence map›Paper›PMID 30386909›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2018

Hypoxia-inducible factor-1α regulation of myeloid cells.

C L Stothers, L Luan, B A Fensterheim, J K Bohannon

Abstract readReview
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Myeloid metabolism and its role in immunotherapy of cancer.Journal for immunotherapy of cancer · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Cigarette smoke-induced airspace disease in mice develops independently of HIF-1α signaling in leukocytes.American journal of physiology. Lung cellular and molecular physiology · 2022
    Article
  13. Article
  14. Article
  15. Oxygen-sensing mechanisms in development and tissue repair.Development (Cambridge, England) · 2021
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review
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

4 authors at 2 institutions in 1 country.

C L StothersDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN, USA. Cody.L.Stothers@Vanderbilt.Edu.
L LuanDepartment of Anesthesiology, Vanderbilt University Medical Center, Nashville, TN, USA.
B A FensterheimDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN, USA.
J K BohannonDepartment of Anesthesiology, Vanderbilt University Medical Center, Nashville, TN, USA.
Vanderbilt University · USVanderbilt University Medical Center · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007347 · NIGMS · VANDERBILT UNIVERSITY · PI WILLIAMS, CHRISTOPHER S. · 1985 to 2023
$26.3M
Enhancing Resistance to Infection after Burn Injury with TLR AgonistsR01GM121711 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BOHANNON, JULIA K. · 2017 to 2021
$1.6M
NIGMS NIH HHS R01 GM121711NIGMS NIH HHS T32 GM007347
6 · The paper itself

Abstract

Hematopoietic myeloblasts give rise to macrophages, dendritic cells, and neutrophils. Circulating myeloid cells detect invading microbes using pattern recognition receptors and subsequently orchestrate an innate immune response to contain and kill the pathogens. This innate immune response establishes an inflammatory niche characterized by hypoxia due to host and pathogen factors. Hypoxia-inducible factor (HIF) transcription factors are the primary regulators of the myeloid response to hypoxia. In particular, HIF-1α is a critical hub that integrates hypoxic and immunogenic signals during infection or inflammation. Hypoxia induces HIF-1α stabilization, which drives metabolic and phenotypic reprogramming of myeloid cells to maximize antimicrobial potential. HIF-1α activity in myeloid-derived cells enhances the host response to infection, but may also play a role in pathogenic inflammatory processes, such as atherosclerosis. In this review, we summarize recent advances that have elucidated the mechanism by which myeloid cells regulate HIF-1α activity and, in turn, how HIF-1α shapes myeloid cell function.

Indexed as

AnimalsAtherosclerosisHumansHypoxia-Inducible Factor 1, alpha SubunitMyeloid CellsHypoxia-Inducible Factor 1, alpha SubunitHIFHypoxiaImmunometabolismInflammationMyeloid

Identifiers

PMID30386909
PMCPMC6292431
OpenAlexW2898840093

What OpenQuestion holds

Textmetadata
LicenceTDM
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.