Evidence map›Paper›PMID 29435987›Full record

ReviewThe Journal of physiology2018

The PHD1 oxygen sensor in health and disease.

Kilian B Kennel, Julius Burmeister, Martin Schneider, Cormac T Taylor

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

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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 2 countries.

Kilian B KennelDepartment of General, Visceral and Transplantation Surgery, University of Heidelberg, Heidelberg, Germany.
Julius BurmeisterDepartment of General, Visceral and Transplantation Surgery, University of Heidelberg, Heidelberg, Germany.
Martin SchneiderDepartment of General, Visceral and Transplantation Surgery, University of Heidelberg, Heidelberg, Germany.
Cormac T TaylorUCD Conway Institute & School of Medicine, University College Dublin, Belfield, Dublin 4, Ireland.ORCID 0000-0002-0946-1247
Heidelberg University · DEUniversity College Dublin · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hypoxia-inducible factor (HIF) co-ordinates the adaptive transcriptional response to hypoxia in metazoan cells. The hypoxic sensitivity of HIF is conferred by a family of oxygen-sensing enzymes termed HIF hydroxylases. This family consists of three prolyl hydroxylases (PHD1-3) and a single asparagine hydroxylase termed factor inhibiting HIF (FIH). It has recently become clear that HIF hydroxylases are functionally non-redundant and have discrete but overlapping physiological roles. Furthermore, altered abundance or activity of these enzymes is associated with a number of pathologies. Pharmacological HIF-hydroxylase inhibitors have recently proven to be both tolerated and therapeutically effective in patients. In this review, we focus on the physiology, pathophysiology and therapeutic potential of the PHD1 isoform, which has recently been implicated in diseases including inflammatory bowel disease, ischaemia and cancer.

Indexed as

Biosensing TechniquesHypoxiaAnimalsHumansHypoxia-Inducible Factor-Proline DioxygenasesInflammatory Bowel DiseasesIschemiaNeoplasmsOxygenHypoxia-Inducible Factor-Proline DioxygenasesOxygenapoptosiscancercolitisHIFhypoxia-inducible factorinflammatory bowel diseaseischemiaNF-κBPHD1PHD inhibitorProlyl-hydroxylase 1

Identifiers

PMID29435987
PMCPMC6117546
OpenAlexW2797027795

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.