Evidence map›Paper›PMID 28680565›Full record

ArticlePulmonary circulation2017

Oxidative injury of the pulmonary circulation in the perinatal period: Short- and long-term consequences for the human cardiopulmonary system.

Daphne P de Wijs-Meijler, Dirk J Duncker, Dick Tibboel, Ralph T Schermuly, Norbert Weissmann, Daphne Merkus, Irwin K M Reiss

Open access · hybridAbstract read
In one paragraph

Article in Pulmonary circulation, 2017. 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
2.0field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 28 citations in OpenAlex.

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  13. Bronchopulmonary Dysplasia and Pulmonary Hypertension. The Role of Smooth MuscleAmerican journal of respiratory cell and molecular biology · 2021
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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 4 institutions in 2 countries.

Daphne P de Wijs-MeijlerDivision of Experimental Cardiology, Department of Cardiology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands.
Dirk J DunckerDivision of Experimental Cardiology, Department of Cardiology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands.
Dick TibboelIntensive Care Unit, Department of Pediatric Surgery, Sophia Children's Hospital, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands.
Ralph T SchermulyUniversity of Giessen and Marburg Lung Center (UGMLC), Excellence Cluster Cardio-Pulmonary Systems (ECCPS), Department of Internal Medicine, Members of the German Center for Lung Research, Justus-Liebig-University, Giessen, Germany.
Norbert WeissmannUniversity of Giessen and Marburg Lung Center (UGMLC), Excellence Cluster Cardio-Pulmonary Systems (ECCPS), Department of Internal Medicine, Members of the German Center for Lung Research, Justus-Liebig-University, Giessen, Germany.
Daphne MerkusDivision of Experimental Cardiology, Department of Cardiology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands.
Irwin K M ReissDivision of Neonatology, Department of Pediatrics, Sophia Children's Hospital, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands.
Erasmus MC · NLErasmus MC - Sophia Children’s Hospital · NLJustus-Liebig-Universität Gießen · DEUniversities of Giessen and Marburg Lung Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Development of the pulmonary circulation is a complex process with a spatial pattern that is tightly controlled. This process is vulnerable for disruption by various events in the prenatal and early postnatal periods. Disruption of normal pulmonary vascular development leads to abnormal structure and function of the lung vasculature, causing neonatal pulmonary vascular diseases. Premature babies are especially at risk of the development of these diseases, including persistent pulmonary hypertension and bronchopulmonary dysplasia. Reactive oxygen species play a key role in the pathogenesis of neonatal pulmonary vascular diseases and can be caused by hyperoxia, mechanical ventilation, hypoxia, and inflammation. Besides the well-established short-term consequences, exposure of the developing lung to injurious stimuli in the perinatal period, including oxidative stress, may also contribute to the development of pulmonary vascular diseases later in life, through so-called "fetal or perinatal programming." Because of these long-term consequences, it is important to develop a follow-up program tailored to adolescent survivors of neonatal pulmonary vascular diseases, aimed at early detection of adult pulmonary vascular diseases, and thereby opening the possibility of early intervention and interfering with disease progression. This review focuses on pathophysiologic events in the perinatal period that have been shown to disrupt human normal pulmonary vascular development, leading to neonatal pulmonary vascular diseases that can extend even into adulthood. This knowledge may be particularly important for ex-premature adults who are at risk of the long-term consequences of pulmonary vascular diseases, thereby contributing disproportionately to the burden of adult cardiovascular disease in the future.

Indexed as

lung developmentoxidative stressoxygenpulmonary circulationpulmonary vascular disease

Identifiers

PMID28680565
PMCPMC5448552
OpenAlexW2531115524

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.