Evidence map›Paper›PMID 30338885›Full record

ReviewEuropean journal of heart failure2019

Treating oxidative stress in heart failure: past, present and future.

Atze van der Pol, Wiek H van Gilst, Adriaan A Voors, Peter van der Meer

Abstract readReview
In one paragraph

Review in European journal of heart failure, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 445 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
445citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

445 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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385 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

4 authors.

Atze van der PolDepartment of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Wiek H van GilstDepartment of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Adriaan A VoorsDepartment of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Peter van der MeerDepartment of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Advances in cardiovascular research have identified oxidative stress as an important pathophysiological pathway in the development and progression of heart failure. Oxidative stress is defined as the imbalance between the production of reactive oxygen species (ROS) and the endogenous antioxidant defence system. Under physiological conditions, small quantities of ROS are produced intracellularly, which function in cell signalling, and can be readily reduced by the antioxidant defence system. However, under pathophysiological conditions, the production of ROS exceeds the buffering capacity of the antioxidant defence system, resulting in cell damage and death. Over the last decades several studies have tried to target oxidative stress with the aim to improve outcome in patients with heart failure, with very limited success. The reasons as to why these studies failed to demonstrate any beneficial effects remain unclear. However, one plausible explanation might be that currently employed strategies, which target oxidative stress by exogenous inhibition of ROS production or supplementation of exogenous antioxidants, are not effective enough, while bolstering the endogenous antioxidant capacity might be a far more potent avenue for therapeutic intervention. In this review, we provide an overview of oxidative stress in the pathophysiology of heart failure and the strategies utilized to date to target this pathway. We provide novel insights into modulation of endogenous antioxidants, which may lead to novel therapeutic strategies to improve outcome in patients with heart failure.

Indexed as

AnimalsAntioxidantsDisease Models, AnimalHeart FailureHumansOxidative StressReactive Oxygen SpeciesAntioxidantsReactive Oxygen SpeciesGlutathioneHeart failureNicotinamide adenine dinucleotideOxidative stressγ-Glutamyl cycle

Identifiers

PMID30338885
PMCPMC6607515

What OpenQuestion holds

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Registered trials

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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.