Evidence map›Paper›PMID 27915400›Full record

ReviewHigh blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension2016

The Pathophysiological Role of NOX2 in Hypertension and Organ Damage.

Maurizio Forte, Cristina Nocella, Elena De Falco, Silvia Palmerio, Leonardo Schirone, Valentina Valenti, Giacomo Frati, Roberto Carnevale, Sebastiano Sciarretta

Abstract readReview
PubMed Publisher
In one paragraph

Review in High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. NADPCurrent medicinal chemistry · 2025
    Review
  4. Article
  5. Review
  6. Angiotensin II acts through Rac1 to upregulate pendrin: role of NADPH oxidase.American journal of physiology. Renal physiology · 2024
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Antioxidants (Basel, Switzerland) · 2021
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article
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

9 authors at 3 institutions in 1 country.

Maurizio ForteDepartment of Angiocardioneurology, IRCCS Neuromed, Pozzilli, 86077, Italy.
Cristina NocellaDepartment of Medical and Surgical Sciences and Biotechnologies, Sapienza University of Rome, 79 Corso della Repubblica, 04100, Latina, Italy.
Elena De FalcoDepartment of Medical and Surgical Sciences and Biotechnologies, Sapienza University of Rome, 79 Corso della Repubblica, 04100, Latina, Italy.
Silvia PalmerioDepartment of Medical and Surgical Sciences and Biotechnologies, Sapienza University of Rome, 79 Corso della Repubblica, 04100, Latina, Italy.
Leonardo SchironeDepartment of Medical and Surgical Sciences and Biotechnologies, Sapienza University of Rome, 79 Corso della Repubblica, 04100, Latina, Italy.
Valentina ValentiDepartment of Imaging, Bambino Gesù Children Hospital, IRCCS, Rome, Italy.
Giacomo FratiDepartment of Angiocardioneurology, IRCCS Neuromed, Pozzilli, 86077, Italy.
Roberto CarnevaleDepartment of Angiocardioneurology, IRCCS Neuromed, Pozzilli, 86077, Italy.
Sebastiano SciarrettaDepartment of Angiocardioneurology, IRCCS Neuromed, Pozzilli, 86077, Italy. sebastiano.sciarretta@uniroma1.it.ORCID http://orcid.org/0000-0002-8633-6896
Istituto Neurologico Mediterraneo · ITSapienza University of Rome · ITBambino Gesù Children's Hospital · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NADPH oxidases (NOXs) represent one of the major sources of reactive oxygen species in the vascular district. Reactive oxygen species are responsible for vascular damage that leads to several cardiovascular pathological conditions. Among NOX isoforms, NOX2 is widely expressed in many cells types, such as cardiomyocytes, endothelial cells, and vascular smooth muscle cells, confirming its pivotal role in vascular pathophysiology. Studies in mice models with systemic deletion of NOX2, as well as in transgenic mice overexpressing NOX2, have demonstrated the undeniable involvement of NOX2 in the development of hypertension, atherosclerosis, diabetes mellitus, cardiac hypertrophy, platelet aggregation, and aging. Of note, the inhibition of NOX2 has been found to be protective for cardiovascular homeostasis. Here, we review the evidence demonstrating that the modulation of NOX2 activity is able to improve vascular physiology, suggesting that NOX2 may be a potential target for therapeutic applications.

Indexed as

Blood PressureAnimalsCardiomegalyFibrosisHumansHypertensionMembrane GlycoproteinsMice, TransgenicMyocardiumNADPH Oxidase 2NADPH OxidasesPlatelet ActivationSignal TransductionUp-RegulationVascular RemodelingVentricular RemodelingCYBB protein, humanCybb protein, mouseMembrane GlycoproteinsNADPH Oxidase 2NADPH OxidasesCardiac hypertrophyHypertensionNADPH oxidaseNOX2Reactive oxygen species

Identifiers

PMID27915400
OpenAlexW2557745916

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.