Evidence map›Paper›PMID 31487802›Full record

ReviewNutrients2019

Oxidative Stress in Cardiovascular Diseases: Still a Therapeutic Target?

Thomas Senoner, Wolfgang Dichtl

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 438 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
438citing papers in PubMed, 2 pooled it
30.0field-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

438 citing papers in PubMed, 2 syntheses or guidelines pooled it, 835 citations in OpenAlex.

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378 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 1 institution in 1 country.

Thomas SenonerDepartment of Internal Medicine III, Cardiology and Angiology, Innsbruck Medical University, Anichstraße 35, 6020 Innsbruck, Austria. Thomas.Senoner@i-med.ac.at.ORCID 0000-0001-5711-244X
Wolfgang DichtlDepartment of Internal Medicine III, Cardiology and Angiology, Innsbruck Medical University, Anichstraße 35, 6020 Innsbruck, Austria. Wolfgang.Dichtl@i-med.ac.at.
Innsbruck Medical University · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular diseases (CVD) are complex entities with heterogenous pathophysiologic mechanisms and increased oxidative stress has been viewed as one of the potential common etiologies. A fine balance between the presence of reactive oxygen species (ROS) and antioxidants is essential for the proper normal functioning of the cell. A basal concentration of ROS is indispensable for the manifestation of cellular functions, whereas excessive levels of ROS cause damage to cellular macromolecules such as DNA, lipids and proteins, eventually leading to necrosis and apoptotic cell death. CVD is the main cause of death worldwide with several conditions being affected by oxidative stress. Increased ROS lead to decreased nitric oxide availability and vasoconstriction, promoting arterial hypertension. ROS also negatively influence myocardial calcium handling, causing arrhythmia, and augment cardiac remodeling by inducing hypertrophic signaling and apoptosis. Finally, ROS have also been shown to promote atherosclerotic plaque formation. This review aims at giving an introduction into oxidative stress in CVD, with special focus on endothelial dysfunction, and then examining in detail the role of oxidative stress in the most prevalent of these diseases. Finally, potential nutraceuticals and diets that might be beneficial in diminishing the burden of oxidative stress in CVD are presented.

Indexed as

DietDietary SupplementsCardiovascular DiseasesHumansInflammationOxidative Stressantioxidantscardiovascular diseasesnutraceuticalsoxidative stress

Identifiers

PMID31487802
PMCPMC6769522
OpenAlexW2971456522

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.