Evidence map›Paper›PMID 26484802›Full record

ReviewRedox biology2015

Reperfusion injury and reactive oxygen species: The evolution of a concept.

D Neil Granger, Peter R Kvietys

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 748 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
748citing papers in PubMed, 6 pooled it
42.8field-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

748 citing papers in PubMed, 6 syntheses or guidelines pooled it, 1,411 citations in OpenAlex.

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688 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 at 2 institutions in 2 countries.

D Neil GrangerDepartment of Molecular & Cellular Physiology, Louisiana State University Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71130-3932, United States. Electronic address: dgrang@lsuhsc.edu.
Peter R KvietysDepartment of Physiological Sciences, College of Medicine, Alfaisal University, Riyadh, Saudi Arabia.
Alfaisal University · SALouisiana State University Health Sciences Center Shreveport · US

Funding

TRANSCAPILLARY FLUID EXCHANGER01HL026441 · NHLBI · UNIVERSITY OF SOUTH ALABAMA · PI GRANGER, D. NEIL · 1985 to 2013
$4.0M
NHLBI NIH HHS HL26441-32NHLBI NIH HHS R01 HL026441
6 · The paper itself

Abstract

Reperfusion injury, the paradoxical tissue response that is manifested by blood flow-deprived and oxygen-starved organs following the restoration of blood flow and tissue oxygenation, has been a focus of basic and clinical research for over 4-decades. While a variety of molecular mechanisms have been proposed to explain this phenomenon, excess production of reactive oxygen species (ROS) continues to receive much attention as a critical factor in the genesis of reperfusion injury. As a consequence, considerable effort has been devoted to identifying the dominant cellular and enzymatic sources of excess ROS production following ischemia-reperfusion (I/R). Of the potential ROS sources described to date, xanthine oxidase, NADPH oxidase (Nox), mitochondria, and uncoupled nitric oxide synthase have gained a status as the most likely contributors to reperfusion-induced oxidative stress and represent priority targets for therapeutic intervention against reperfusion-induced organ dysfunction and tissue damage. Although all four enzymatic sources are present in most tissues and are likely to play some role in reperfusion injury, priority and emphasis has been given to specific ROS sources that are enriched in certain tissues, such as xanthine oxidase in the gastrointestinal tract and mitochondria in the metabolically active heart and brain. The possibility that multiple ROS sources contribute to reperfusion injury in most tissues is supported by evidence demonstrating that redox-signaling enables ROS produced by one enzymatic source (e.g., Nox) to activate and enhance ROS production by a second source (e.g., mitochondria). This review provides a synopsis of the evidence implicating ROS in reperfusion injury, the clinical implications of this phenomenon, and summarizes current understanding of the four most frequently invoked enzymatic sources of ROS production in post-ischemic tissue.

Indexed as

AnimalsCell HypoxiaHumansOxidation-ReductionOxidative StressReactive Oxygen SpeciesReperfusion InjuryReactive Oxygen SpeciesHypoxia-reoxygenationIschemia-reperfusionMitochondriaNADPH oxidaseUncoupled nitric oxide synthaseXanthine oxidase

Identifiers

PMID26484802
PMCPMC4625011
OpenAlexW1809795104

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.