Evidence map›Paper›PMID 30364203›Full record

ReviewFrontiers in cell and developmental biology2018

Reactive Oxygen Species Formation in the Brain at Different Oxygen Levels: The Role of Hypoxia Inducible Factors.

Ruoli Chen, U Hin Lai, Lingling Zhu, Ayesha Singh, Muhammad Ahmed, Nicholas R Forsyth

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed, 1 pooled it
7.3field-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

151 citing papers in PubMed, 1 synthesis or guideline pooled it, 257 citations in OpenAlex.

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91 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

6 authors at 3 institutions in 2 countries.

Ruoli ChenSchool of Pharmacy, Keele University, Staffordshire, United Kingdom.
U Hin LaiSchool of Pharmacy, Keele University, Staffordshire, United Kingdom.
Lingling ZhuDepartment of Brain Protection and Plasticity, Institute of Basic Medical Sciences, Beijing, China.
Ayesha SinghSchool of Pharmacy, Keele University, Staffordshire, United Kingdom.
Muhammad AhmedInstitute for Science and Technology in Medicine, Keele University, Staffordshire, United Kingdom.
Nicholas R ForsythInstitute for Science and Technology in Medicine, Keele University, Staffordshire, United Kingdom.
Keele University · GBInstitute of Basic Medical Sciences of the Chinese Academy of Medical SciencesUniversity of Mosul · IQ

Funding

Wellcome Trust
6 · The paper itself

Abstract

Hypoxia inducible factor (HIF) is the master oxygen sensor within cells and is central to the regulation of cell responses to varying oxygen levels. HIF activation during hypoxia ensures optimum ATP production and cell integrity, and is associated both directly and indirectly with reactive oxygen species (ROS) formation. HIF activation can either reduce ROS formation by suppressing the function of mitochondrial tricarboxylic acid cycle (TCA cycle), or increase ROS formation via NADPH oxidase (NOX), a target gene of HIF pathway. ROS is an unavoidable consequence of aerobic metabolism. In normal conditions (i.e., physioxia), ROS is produced at minimal levels and acts as a signaling molecule subject to the dedicated balance between ROS production and scavenging. Changes in oxygen concentrations affect ROS formation. When ROS levels exceed defense mechanisms, ROS causes oxidative stress. Increased ROS levels can also be a contributing factor to HIF stabilization during hypoxia and reoxygenation. In this review, we systemically review HIF activation and ROS formation in the brain during hypoxia and hypoxia/reoxygenation. We will then explore the literature describing how changes in HIF levels might provide pharmacological targets for effective ischaemic stroke treatment. HIF accumulation in the brain via HIF prolyl hydroxylase (PHD) inhibition is proposed as an effective therapy for ischaemia stroke due to its antioxidation and anti-inflammatory properties in addition to HIF pro-survival signaling. PHD is a key regulator of HIF levels in cells. Pharmacological inhibition of PHD increases HIF levels in normoxia (i.e., at 20.9% O

Indexed as

brainhypoxiahypoxia inducible factorprolyl hydroxylasereactive oxygen speciesreperfusionstroke

Identifiers

PMID30364203
PMCPMC6192379
OpenAlexW2894357210

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.