Evidence map›Paper›PMID 32408480›Full record

ReviewInternational journal of molecular sciences2020

Regulation of Vascular Function and Inflammation via Cross Talk of Reactive Oxygen and Nitrogen Species from Mitochondria or NADPH Oxidase-Implications for Diabetes Progression.

Andreas Daiber, Sebastian Steven, Ksenija Vujacic-Mirski, Sanela Kalinovic, Matthias Oelze, Fabio Di Lisa, Thomas Münzel

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 51 citations in OpenAlex.

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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

7 authors at 2 institutions in 2 countries.

Andreas DaiberCenter for Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg University, 55131 Mainz, Germany.ORCID 0000-0002-2769-0094
Sebastian StevenCenter for Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg University, 55131 Mainz, Germany.
Ksenija Vujacic-MirskiCenter for Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg University, 55131 Mainz, Germany.ORCID 0000-0002-4800-4209
Sanela KalinovicCenter for Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg University, 55131 Mainz, Germany.ORCID 0000-0002-8401-2425
Matthias OelzeCenter for Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg University, 55131 Mainz, Germany.
Fabio Di LisaDepartment of Biomedical Sciences, University of Padova, 35131 Padova, Italy.
Thomas MünzelCenter for Cardiology, Department of Cardiology 1, University Medical Center of the Johannes Gutenberg University, 55131 Mainz, Germany.ORCID 0000-0001-5503-4150
Johannes Gutenberg University Mainz · DEUniversity of Padua · IT

Funding

Boehringer Ingelheim Stiftung Novel and neglected cardiovascular risk factors: molecular mechanisms and therapeuticsDeutsches Zentrum für Herz-Kreislaufforschung Partner Site Rhine-Main, MainzEuropean Cooperation in Science and Technology EU-CARDIOPROTECTION COST-ACTION (CA16225)
6 · The paper itself

Abstract

Oxidative stress plays a key role for the development of cardiovascular, metabolic, and neurodegenerative disease. This concept has been proven by using the approach of genetic deletion of reactive oxygen and nitrogen species (RONS) producing, pro-oxidant enzymes as well as by the overexpression of RONS detoxifying, antioxidant enzymes leading to an amelioration of the severity of diseases. Vice versa, the development and progression of cardiovascular diseases is aggravated by overexpression of RONS producing enzymes as well as deletion of RONS detoxifying enzymes. We have previously identified cross talk mechanisms between different sources of RONS, which can amplify the oxidative stress-mediated damage. Here, the pathways and potential mechanisms leading to this cross talk are analyzed in detail and highlighted by selected examples from the current literature and own data including hypoxia, angiotensin II (AT-II)-induced hypertension, nitrate tolerance, aging, and others. The general concept of redox-based activation of RONS sources via "kindling radicals" and enzyme-specific "redox switches" as well as the interaction with redox-sensitive inflammatory pathways are discussed. Here, we present evidence for the existence of such cross talk mechanisms in the setting of diabetes and critically assess their contribution to the severity of diabetic complications.

Indexed as

AnimalsCardiovascular DiseasesDiabetes MellitusDisease ProgressionHumansInflammationMitochondriaNADPH OxidasesReactive Nitrogen SpeciesReactive Oxygen SpeciesNADPH OxidasesReactive Nitrogen SpeciesReactive Oxygen Speciesendothelial dysfunctioneNOS uncouplingkindling radicalslow-grade inflammationmitochondriaNADPH oxidaseoxidative stressredox cross talk

Identifiers

PMID32408480
PMCPMC7279344
OpenAlexW3024773476

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.