Evidence map›Paper›PMID 30277804›Full record

ArticleAmerican journal of respiratory cell and molecular biology2019

Nitric Oxide Synthase 2 Induction Promotes Right Ventricular Fibrosis.

Mario Boehm, Tatyana Novoyatleva, Baktybek Kojonazarov, Florian Veit, Norbert Weissmann, Hossein A Ghofrani, Werner Seeger, Ralph T Schermuly

RetractedAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Retraction: Nitric Oxide Synthase 2 Induction Promotes Right Ventricular Fibrosis.American journal of respiratory cell and molecular biology · 2022
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Role of PI3K/Akt signaling pathway in cardiac fibrosis.Molecular and cellular biochemistry · 2021
    Review
  8. Review
  9. Heart Rate Reduction by Ivabradine: Slowly but Surely?American journal of respiratory cell and molecular biology · 2020
    Article
  10. Cardioprotection in right heart failure.British journal of pharmacology · 2020
    Review
  11. Emerging therapies for right ventricular dysfunction and failure.Cardiovascular diagnosis and therapy · 2020
    Review
  12. Article
  13. Update in Pulmonary Vascular Diseases and Right Ventricular Dysfunction 2019.American journal of respiratory and critical care medicine · 2020
    Article
  14. Review
  15. Article
  16. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Mario Boehm1 Universities of Giessen and Marburg Lung Center, Giessen, Germany.
Tatyana Novoyatleva1 Universities of Giessen and Marburg Lung Center, Giessen, Germany.
Baktybek Kojonazarov1 Universities of Giessen and Marburg Lung Center, Giessen, Germany.
Florian Veit1 Universities of Giessen and Marburg Lung Center, Giessen, Germany.
Norbert Weissmann1 Universities of Giessen and Marburg Lung Center, Giessen, Germany.
Hossein A Ghofrani1 Universities of Giessen and Marburg Lung Center, Giessen, Germany.
Werner Seeger1 Universities of Giessen and Marburg Lung Center, Giessen, Germany.
Ralph T Schermuly1 Universities of Giessen and Marburg Lung Center, Giessen, Germany.
Cardio-Pulmonary Institute · DEUniversities of Giessen and Marburg Lung Center · DEGerman Center for Lung Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ability of the right ventricle to compensate pressure overload determines survival in pulmonary arterial hypertension (PAH). Nitric oxide (NO) reduces the right ventricular afterload through pulmonary vasodilation, but excessive NO amounts cause oxidative stress. Oxidative stress drives remodeling of pulmonary arteries and the right ventricle. In the present study, we hypothesized that nitric oxide synthase 2 (NOS2) induction leads to excessive NO amounts that contribute to oxidative stress and impair right ventricular adaptation to PAH. We used a surgical pulmonary artery banding (PAB) mouse model in which right ventricular dysfunction and remodeling occur independently of changes in the pulmonary vasculature. Three weeks after PAB, NOS2 expression was increased twofold in the hypertrophied right ventricle on transcript and protein levels together with increased NO production. Histomorphology localized NOS2 in interstitial and perivascular cardiac fibroblasts after PAB, which was confirmed by cell isolation experiments. In the hypertrophied right ventricle, NOS2 induction was accompanied by an increased formation of reactive oxidants blocked by ex vivo NOS inhibition. We show that reactive oxidant formation in the hypertrophied right ventricle is in part NOS2 dependent (in NOS2-deficient mice [NOS2

Indexed as

AnimalsDisease Models, AnimalFibrosisHeart VentriclesHypertension, PulmonaryHypertrophy, Right VentricularMaleMice, Inbred C57BLNitric OxideNitric Oxide Synthase Type IIOxidative StressPulmonary ArteryVentricular Dysfunction, RightVentricular Function, RightVentricular RemodelingNitric OxideNitric Oxide Synthase Type IINos2 protein, mousecardiac fibrosisnitric oxide synthasepulmonary hypertensionright ventricle

Identifiers

PMID30277804
OpenAlexW2894947304

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.