Evidence map›Paper›PMID 30190678›Full record

ReviewFrontiers in physiology2018

The Regulation of Pulmonary Vascular Tone by Neuropeptides and the Implications for Pulmonary Hypertension.

Charmaine C W Lo, Seyed M Moosavi, Kristen J Bubb

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Role of Sensory Nerves in Pulmonary Fibrosis.International journal of molecular sciences · 2024
    Review
  6. Review
  7. Review
  8. Endotyping COPD: hypoxia-inducible factor-2 as a molecular "switch" between the vascular and airway phenotypes?European respiratory review : an official journal of the European Respiratory Society · 2023
    Review
  9. Article
  10. Observational
  11. Mechanisms of pulmonary vascular dysfunction in pulmonary hypertension and implications for novel therapies.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  12. The crucial role of prolactin-lactogenic hormone in Covid-19.Molecular and cellular biochemistry · 2022
    Review
  13. Review
  14. Review
  15. Article
  16. The role of cytochrome P450 (CYP) enzymes in hyperoxic lung injury.Expert opinion on drug metabolism & toxicology · 2021
    Review
  17. Pulmonary Sensory Receptors.Advances in anatomy, embryology, and cell biology · 2021
    Article
  18. The Pulmonary NEB ME Is a Complex Intraepithelial Unit.Advances in anatomy, embryology, and cell biology · 2021
    Article
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

Charmaine C W LoKolling Institute of Medical Research, University of Sydney, St Leonards, NSW, Australia.
Seyed M MoosaviKolling Institute of Medical Research, University of Sydney, St Leonards, NSW, Australia.
Kristen J BubbKolling Institute of Medical Research, University of Sydney, St Leonards, NSW, Australia.
University of Sydney · AUUniversity of Technology Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary hypertension (PH) is an incurable, chronic disease of small pulmonary vessels. Progressive remodeling of the pulmonary vasculature results in increased pulmonary vascular resistance (PVR). This causes secondary right heart failure. PVR is tightly regulated by a range of pulmonary vasodilators and constrictors. Endothelium-derived substances form the basis of most current PH treatments. This is particularly the case for pulmonary arterial hypertension. The major limitation of current treatments is their inability to reverse morphological changes. Thus, there is an unmet need for novel therapies to reduce the morbidity and mortality in PH. Microvessels in the lungs are highly innervated by sensory C fibers. Substance P and calcitonin gene-related peptide (CGRP) are released from C-fiber nerve endings. These neuropeptides can directly regulate vascular tone. Substance P tends to act as a vasoconstrictor in the pulmonary circulation and it increases in the lungs during experimental PH. The receptor for substance P, neurokinin 1 (NK1R), mediates increased pulmonary pressure. Deactivation of NK1R with antagonists, or depletion of substance P prevents PH development. CGRP is a potent pulmonary vasodilator. CGRP receptor antagonists cause elevated pulmonary pressure. Thus, the balance of these peptides is crucial within the pulmonary circulation (

Indexed as

calcitonin gene-related peptideendothelial functionlungpulmonary hypertensionright ventriclesensory C fiberssubstance P

Identifiers

PMID30190678
PMCPMC6116211
OpenAlexW2888129838

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.