Evidence map›Paper›PMID 32389339›Full record

ReviewThe Canadian journal of cardiology2020

Oxidative Stress: A Unifying Paradigm in Hypertension.

Rhian M Touyz, Francisco J Rios, Rhéure Alves-Lopes, Karla B Neves, Livia L Camargo, Augusto C Montezano

Open access · hybridAbstract readReview
In one paragraph

Review in The Canadian journal of cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed, 2 pooled it
18.8field-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

148 citing papers in PubMed, 2 syntheses or guidelines pooled it, 255 citations in OpenAlex.

  1. Pooled it
  2. Serum Malondialdehyde Levels in Hypertensive Patients: A Non-invasive Marker of Oxidative Stress. A Systematic Review and Meta-analysis.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2022
    Pooled it
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88 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

6 authors at 2 institutions in 1 country.

Rhian M TouyzInstitute of Cardiovascular and Medical Sciences, British Heart Foundation Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland, United Kingdom. Electronic address: rhian.touyz@glasgow.ac.uk.
Francisco J RiosInstitute of Cardiovascular and Medical Sciences, British Heart Foundation Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland, United Kingdom.
Rhéure Alves-LopesInstitute of Cardiovascular and Medical Sciences, British Heart Foundation Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland, United Kingdom.
Karla B NevesInstitute of Cardiovascular and Medical Sciences, British Heart Foundation Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland, United Kingdom.
Livia L CamargoInstitute of Cardiovascular and Medical Sciences, British Heart Foundation Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland, United Kingdom.
Augusto C MontezanoInstitute of Cardiovascular and Medical Sciences, British Heart Foundation Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland, United Kingdom.
University of Glasgow · GBBritish Heart Foundation · GB

Funding

British Heart Foundation CH/12/29762British Heart Foundation RE/18/6/34217
6 · The paper itself

Abstract

The etiology of hypertension involves complex interactions among genetic, environmental, and pathophysiologic factors that influence many regulatory systems. Hypertension is characteristically associated with vascular dysfunction, cardiovascular remodelling, renal dysfunction, and stimulation of the sympathetic nervous system. Emerging evidence indicates that the immune system is also important and that activated immune cells migrate and accumulate in tissues promoting inflammation, fibrosis, and target-organ damage. Common to these processes is oxidative stress, defined as an imbalance between oxidants and antioxidants in favour of the oxidants that leads to a disruption of oxidation-reduction (redox) signalling and control and molecular damage. Physiologically, reactive oxygen species (ROS) act as signalling molecules and influence cell function through highly regulated redox-sensitive signal transduction. In hypertension, oxidative stress promotes posttranslational modification (oxidation and phosphorylation) of proteins and aberrant signalling with consequent cell and tissue damage. Many enzymatic systems generate ROS, but NADPH oxidases (Nox) are the major sources in cells of the heart, vessels, kidneys, and immune system. Expression and activity of Nox are increased in hypertension and are the major systems responsible for oxidative stress in cardiovascular disease. Here we provide a unifying concept where oxidative stress is a common mediator underlying pathophysiologic processes in hypertension. We focus on some novel concepts whereby ROS influence vascular function, aldosterone/mineralocorticoid actions, and immunoinflammation, all important processes contributing to the development of hypertension.

Indexed as

AldosteroneAngiotensin IIEndothelin-1Endothelium, VascularHumansHypertensionInflammationIntercellular Signaling Peptides and ProteinsOxidation-ReductionOxidative StressReactive Oxygen SpeciesSex FactorsSignal TransductionVascular RemodelingVascular StiffnessVasoconstrictionAldosteroneAngiotensin IIEndothelin-1Intercellular Signaling Peptides and ProteinsReactive Oxygen Species

Identifiers

PMID32389339
PMCPMC7225748
OpenAlexW3008065272

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.