Evidence map›Paper›PMID 37881627›Full record

ReviewFrontiers in medicine2023

Role of prostanoids, nitric oxide and endothelin pathways in pulmonary hypertension due to COPD.

Abdullah A Alqarni, Abdulelah M Aldhahir, Sara A Alghamdi, Jaber S Alqahtani, Rayan A Siraj, Hassan Alwafi, Abdulkareem A AlGarni, Mansour S Majrshi, Saad M Alshehri, Linhua Pang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
2.6field-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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Dietary Beetroot Juice - Effects in Patients with COPD: A Review.International journal of chronic obstructive pulmonary disease · 2024
    Review
  9. Review
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

10 authors at 9 institutions in 2 countries.

Abdullah A AlqarniDepartment of Respiratory Therapy, Faculty of Medical Rehabilitation Sciences, King Abdulaziz University, Jeddah, Saudi Arabia.
Abdulelah M AldhahirRespiratory Therapy Department, Faculty of Applied Medical Sciences, Jazan University, Jazan, Saudi Arabia.
Sara A AlghamdiRespiratory Care Department, Al Murjan Hospital, Jeddah, Saudi Arabia.
Jaber S AlqahtaniDepartment of Respiratory Care, Prince Sultan Military College of Health Sciences, Dammam, Saudi Arabia.
Rayan A SirajDepartment of Respiratory Care, College of Applied Medical Sciences, King Faisal University, Al Ahsa, Saudi Arabia.
Hassan AlwafiFaculty of Medicine, Umm Al-Qura University, Mecca, Saudi Arabia.
Abdulkareem A AlGarniKing Abdulaziz Hospital, The Ministry of National Guard Health Affairs, Al Ahsa, Saudi Arabia.
Mansour S MajrshiNational Heart and Lung Institute, Imperial College London, London, United Kingdom.
Saad M AlshehriDepartment of Respiratory Therapy, King Fahad General Hospital, Jeddah, Saudi Arabia.
Linhua PangRespiratory Medicine Research Group, Academic Unit for Translational Medical Sciences, University of Nottingham School of Medicine, Nottingham, United Kingdom.
Imperial College London · GBJazan University · SAKing Abdulaziz Hospital · SAKing Fahad Hospital Jeddah · SAKing Faisal University · SANational Guard Health Affairs · SAPrince Sultan Military College of Health SciencesUmm al-Qura University · SAUniversity of Nottingham · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary hypertension (PH) due to chronic obstructive pulmonary disease (COPD) is classified as Group 3 PH, with no current proven targeted therapies. Studies suggest that cigarette smoke, the most risk factor for COPD can cause vascular remodelling and eventually PH as a result of dysfunction and proliferation of pulmonary artery smooth muscle cells (PASMCs) and pulmonary artery endothelial cells (PAECs). In addition, hypoxia is a known driver of pulmonary vascular remodelling in COPD, and it is also thought that the presence of hypoxia in patients with COPD may further exaggerate cigarette smoke-induced vascular remodelling; however, the underlying cause is not fully understood. Three main pathways (prostanoids, nitric oxide and endothelin) are currently used as a therapeutic target for the treatment of patients with different groups of PH. However, drugs targeting these three pathways are not approved for patients with COPD-associated PH due to lack of evidence. Thus, this review aims to shed light on the role of impaired prostanoids, nitric oxide and endothelin pathways in cigarette smoke- and hypoxia-induced pulmonary vascular remodelling and also discusses the potential of using these pathways as therapeutic target for patients with PH secondary to COPD.

Indexed as

COPDCOPD-associated pulmonary hypertensionendothelinnitric oxideprostanoidpulmonary hypertensionpulmonary hypertension in COPDtype 3 pulmonary hypertension

Identifiers

PMID37881627
PMCPMC10597708
OpenAlexW4387514170

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.