Evidence map›Paper›PMID 23934926›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013

Soluble guanylate cyclase modulates alveolarization in the newborn lung.

Patricia R Bachiller, Katherine H Cornog, Rina Kato, Emmanuel S Buys, Jesse D Roberts

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Trial
  2. Role of ROS, soluble guanylate cyclase and cGMP in mouse lung development during hyperoxia.American journal of physiology. Heart and circulatory physiology · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. The differential roles of the two NO-GC isoforms in adjusting airway reactivity.American journal of physiology. Lung cellular and molecular physiology · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Antenatal BAY 41-2272 reduces pulmonary hypertension in the rabbit model of congenital diaphragmatic hernia.American journal of physiology. Lung cellular and molecular physiology · 2016
    Article
  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

5 authors.

Patricia R BachillerJr., Cardiovascular Research Center, Massachusetts General Hospital - East, 149 13 St., Charlestown, MA 02129. roberts@cvrc.mgh.harvard.edu.
Katherine H Cornog
Rina Kato
Emmanuel S Buys
Jesse D Roberts

Funding

Mechanisms regulating PKGI proteolysis and modulation of pulmonary SMC phenotypeR01HL096779 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI ROBERTS, JESSE D · 2010 to 2013
$1.7M
NHLBI NIH HHS 1R01HL096779NHLBI NIH HHS R01 HL096779NIGMS NIH HHS 5T32GM0759
6 · The paper itself

Abstract

Nitric oxide (NO) regulates lung development through incompletely understood mechanisms. NO controls pulmonary vascular smooth muscle cell (SMC) differentiation largely through stimulating soluble guanylate cyclase (sGC) to produce cGMP and increase cGMP-mediated signaling. To examine the role of sGC in regulating pulmonary development, we tested whether decreased sGC activity reduces alveolarization in the normal and injured newborn lung. For these studies, mouse pups with gene-targeted sGC-α1 subunit truncation were used because we determined that they have decreased pulmonary sGC enzyme activity. sGC-α1 knockout (KO) mouse pups were observed to have decreased numbers of small airway structures and lung volume compared with wild-type (WT) mice although lung septation and body weights were not different. However, following mild lung injury caused by breathing 70% O2, the sGC-α1 KO mouse pups had pronounced inhibition of alveolarization, as evidenced by an increase in airway mean linear intercept, reduction in terminal airway units, and decrease in lung septation and alveolar openings, as well as reduced somatic growth. Because cGMP regulates SMC phenotype, we also tested whether decreased sGC activity reduces lung myofibroblast differentiation. Cellular markers revealed that vascular SMC differentiation decreased, whereas myofibroblast activation increased in the hyperoxic sGC-α1 KO pup lung. These results indicate that lung development, particularly during hyperoxic injury, is impaired in mouse pups with diminished sGC activity. These studies support the investigation of sGC-targeting agents as therapies directed at improving development in the newborn lung exposed to injury.

Indexed as

AnimalsAnimals, NewbornCell DifferentiationCyclic GMPGuanylate CyclaseHyperoxiaLung InjuryMiceMice, KnockoutMyofibroblastsPulmonary AlveoliReceptors, Cytoplasmic and NuclearSoluble Guanylyl CyclaseCyclic GMPGuanylate CyclaseReceptors, Cytoplasmic and NuclearSoluble Guanylyl CyclasealveolarizationcGMPlung developmentsoluble guanylate cyclase

Identifiers

PMID23934926
PMCPMC3798773

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.