Evidence map›Paper›PMID 23600794›Full record

ReviewAntioxidants & redox signaling2014

Reactive oxygen species, vascular Noxs, and hypertension: focus on translational and clinical research.

Augusto C Montezano, Rhian M Touyz

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed
14.1field-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

119 citing papers in PubMed, 267 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
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  6. Review
  7. Oxidative Stress and Its Role in Vascular Damage and Atherosclerosis.International journal of molecular sciences · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Mitochondrial Dysfunction in Cardiovascular Diseases.International journal of molecular sciences · 2025
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Alpinia zerumbet leaf extract reverses hypertension and improves adverse remodeling in the left ventricle and aorta in spontaneously hypertensive rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025
    Article
  19. Article
  20. Article

59 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.

Augusto C MontezanoInstitute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow , Glasgow, United Kingdom .
Rhian M Touyz
University of Glasgow · GB

Funding

Canadian Institutes of Health Research 44018Canadian Institutes of Health Research 57886
6 · The paper itself

Abstract

significanceReactive oxygen species (ROS) are signaling molecules that are important in physiological processes, including host defense, aging, and cellular homeostasis. Increased ROS bioavailability and altered redox signaling (oxidative stress) have been implicated in the onset and/or progression of chronic diseases, including hypertension. RECENT ADVANCES: Although oxidative stress may not be the only cause of hypertension, it amplifies blood pressure elevation in the presence of other pro-hypertensive factors, such as salt loading, activation of the renin-angiotensin-aldosterone system, and sympathetic hyperactivity, at least in experimental models. A major source for ROS in the cardiovascular-renal system is a family of nicotinamide adenine dinucleotide phosphate oxidases (Noxs), including the prototypic Nox2-based Nox, and Nox family members: Nox1, Nox4, and Nox5. CRITICAL ISSUES: Although extensive experimental data support a role for increased ROS levels and altered redox signaling in the pathogenesis of hypertension, the role in clinical hypertension is unclear, as a direct causative role of ROS in blood pressure elevation has yet to be demonstrated in humans. Nevertheless, what is becoming increasingly evident is that abnormal ROS regulation and aberrant signaling through redox-sensitive pathways are important in the pathophysiological processes which is associated with vascular injury and target-organ damage in hypertension. FUTURE DIRECTIONS: There is a paucity of clinical information related to the mechanisms of oxidative stress and blood pressure elevation, and a few assays accurately measure ROS directly in patients. Such further ROS research is needed in humans and in the development of adequately validated analytical methods to accurately assess oxidative stress in the clinic.

Indexed as

AnimalsAntihypertensive AgentsAntioxidantsBiomedical ResearchBlood VesselsDisease Models, AnimalHumansHypertensionNADPH OxidasesOxidative StressReactive Oxygen SpeciesTranslational Research, BiomedicalAntihypertensive AgentsAntioxidantsNADPH OxidasesReactive Oxygen Species

Identifiers

PMID23600794
PMCPMC3880913
OpenAlexW2033810451

What OpenQuestion holds

Textmetadata
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.