Evidence map›Paper›PMID 29761172›Full record

ArticleHepatology communications2018

Loss of hypoxia inducible factor-1α aggravates γδ T-cell-mediated inflammation during acetaminophen-induced liver injury.

Tomohiro Suzuki, Shoko Minagawa, Takashi Yamazaki, Takatomo Arai, Mai Kanai, Satoko Shinjo, Nobuhito Goda

Open access · goldAbstract read
In one paragraph

Article in Hepatology communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Hypoxia and HIF Signaling: One Axis with Divergent Effects.International journal of molecular sciences · 2020
    Review
  10. Norepinephrine released by intestinal Paneth cells exacerbates ischemic AKI.American journal of physiology. Renal physiology · 2020
    Article
  11. Hypoxia signaling in human diseases and therapeutic targets.Experimental & molecular medicine · 2019
    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

7 authors at 1 institution in 1 country.

Tomohiro SuzukiDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering Waseda University Tokyo Japan.
Shoko MinagawaDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering Waseda University Tokyo Japan.
Takashi YamazakiDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering Waseda University Tokyo Japan.
Takatomo AraiDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering Waseda University Tokyo Japan.
Mai KanaiDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering Waseda University Tokyo Japan.
Satoko ShinjoDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering Waseda University Tokyo Japan.
Nobuhito GodaDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering Waseda University Tokyo Japan.
Waseda University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acetaminophen (APAP)-induced liver injury is closely associated with acute hepatic inflammation. Hypoxia-inducible factor-1 (HIF-1) is activated during immunological processes and regulates gene expressions in various types of immune cells. Although HIF-1 controls the differentiation and functions of conventional T cells in chronic inflammation, the pathological importance of HIF-1 in innate-like T cells during acute inflammation remains unknown. Here, we investigated the role of HIF-1 in innate-like γδ T cells during APAP-induced acute liver injury. In response to APAP administration, T-cell-specific

Identifiers

PMID29761172
PMCPMC5944581
OpenAlexW2791626659

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.