Evidence map›Paper›PMID 28684719›Full record

ReviewAntioxidants (Basel, Switzerland)2017

Reactive Oxygen and Nitrogen Species in the Development of Pulmonary Hypertension.

David J R Fulton, Xueyi Li, Zsuzsanna Bordan, Stephen Haigh, Austin Bentley, Feng Chen, Scott A Barman

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 73 citations in OpenAlex.

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  10. Endothelial PHD2 deficiency induces nitrative stressThe European respiratory journal · 2022
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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.

David J R FultonVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. DFULTON@augusta.edu.
Xueyi LiVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. xuli@augusta.edu.
Zsuzsanna BordanVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. zbordan@augusta.edu.
Stephen HaighVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. shaigh@augusta.edu.
Austin BentleyVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. aubentley@augusta.edu.
Feng ChenDepartment of Forensic Medicine, Nanjing Medical University, Nanjing 211166, China. fchen@njmu.edu.cn.
Scott A BarmanDepartment of Pharmacology and Toxicology, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. sbarman@augusta.edu.
Augusta University · USNanjing Medical University · CN

Funding

Galectin-3: A mediator of vascular remodeling in pulmonary arterial hypertensionR01HL125926 · NHLBI · AUGUSTA UNIVERSITY · PI BARMAN, SCOTT A, FULTON, DAVID J · 2016 to 2025
$4.9M
Novel mechanistic pathways of cardiovascular disease in obesityR01HL124773 · NHLBI · AUGUSTA UNIVERSITY · PI FULTON, DAVID J, STEPP, DAVID W · 2015 to 2018
$2.2M
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a progressive disease of the lung vasculature that involves the loss of endothelial function together with inappropriate smooth muscle cell growth, inflammation, and fibrosis. These changes underlie a progressive remodeling of blood vessels that alters flow and increases pulmonary blood pressure. Elevated pressures in the pulmonary artery imparts a chronic stress on the right ventricle which undergoes compensatory hypertrophy but eventually fails. How PAH develops remains incompletely understood and evidence for the altered production of reactive oxygen and nitrogen species (ROS, RNS respectively) in the pulmonary circulation has been well documented. There are many different types of ROS and RNS, multiple sources, and collective actions and interactions. This review summarizes past and current knowledge of the sources of ROS and RNS and how they may contribute to the loss of endothelial function and changes in smooth muscle proliferation in the pulmonary circulation.

Indexed as

endothelial nitric oxide synthase (eNOS)nicotinamide adenine dinucleotide phosphate-oxidase (NADPH oxidase)nitric oxideNoxpulmonary hypertensionreactive oxygen species

Identifiers

PMID28684719
PMCPMC5618082
OpenAlexW2726316859

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.