Evidence map›Paper›PMID 26251902›Full record

ReviewInternational journal of molecular sciences2015

Exploiting the Pleiotropic Antioxidant Effects of Established Drugs in Cardiovascular Disease.

Sebastian Steven, Thomas Münzel, Andreas Daiber

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 67 citations in OpenAlex.

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  13. Ref-1 protects against FeClThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021
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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

3 authors at 1 institution in 1 country.

Sebastian StevenMedical Clinic, University Medical Center of the Johannes Gutenberg-University, Mainz 55131, Germany. Sebastiansteven@gmx.de.
Thomas MünzelMedical Clinic, University Medical Center of the Johannes Gutenberg-University, Mainz 55131, Germany. tmuenzel@uni-mainz.de.
Andreas DaiberMedical Clinic, University Medical Center of the Johannes Gutenberg-University, Mainz 55131, Germany. daiber@uni-mainz.de.
Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular disease is a leading cause of death and reduced quality of life worldwide. Arterial vessels are a primary target for endothelial dysfunction and atherosclerosis, which is accompanied or even driven by increased oxidative stress. Recent research in this field identified different sources of reactive oxygen and nitrogen species contributing to the pathogenesis of endothelial dysfunction. According to lessons from the past, improvement of endothelial function and prevention of cardiovascular disease by systemic, unspecific, oral antioxidant therapy are obviously too simplistic an approach. Source- and cell organelle-specific antioxidants as well as activators of intrinsic antioxidant defense systems might be more promising. Since basic research demonstrated the contribution of different inflammatory cells to vascular oxidative stress and clinical trials identified chronic inflammatory disorders as risk factors for cardiovascular events, atherosclerosis and cardiovascular disease are closely associated with inflammation. Therefore, modulation of the inflammatory response is a new and promising approach in the therapy of cardiovascular disease. Classical anti-inflammatory therapeutic compounds, but also established drugs with pleiotropic immunomodulatory abilities, demonstrated protective effects in various models of cardiovascular disease. However, results from ongoing clinical trials are needed to further evaluate the value of immunomodulation for the treatment of cardiovascular disease.

Indexed as

AnimalsAntioxidantsCardiovascular DiseasesEndothelium, VascularGlucagon-Like PeptidesHumansImmunologic FactorsInflammationOxidative StressAntioxidantsGlucagon-Like PeptidesImmunologic Factorscardiovascular diseasedipeptidyl peptidase-4 inhibitorsendothelial dysfunctionglucagon-like peptide analogsinflammationoxidative stress

Identifiers

PMID26251902
PMCPMC4581241
OpenAlexW2121019653

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.