Evidence map›Paper›PMID 35163176›Full record

ReviewInternational journal of molecular sciences2022

The Role of Sphingolipid Signaling in Oxidative Lung Injury and Pathogenesis of Bronchopulmonary Dysplasia.

Jaya M Thomas, Tara Sudhadevi, Prathima Basa, Alison W Ha, Viswanathan Natarajan, Anantha Harijith

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Jaya M ThomasDepartment of Pediatrics, Case Western Reserve University, Cleveland, OH 44106, USA.
Tara SudhadeviDepartment of Pediatrics, Case Western Reserve University, Cleveland, OH 44106, USA.
Prathima BasaDepartment of Pediatrics, Case Western Reserve University, Cleveland, OH 44106, USA.
Alison W HaDepartment of Pediatrics, Case Western Reserve University, Cleveland, OH 44106, USA.
Viswanathan NatarajanDepartment of Pharmacology and Regenerative Medicine, University of Illinois at Chicago, Chicago, IL 60607, USA.ORCID 0000-0002-5132-8212
Anantha HarijithDepartment of Pediatrics, Case Western Reserve University, Cleveland, OH 44106, USA.ORCID 0000-0002-4868-3862
Case Western Reserve University · USUniversity of Illinois Chicago · US

Funding

Role of novel SphK1 inhibitor, PF543 in therapy of Bronchopulmonary dysplasia and Airway remodelingR01HD090887 · NICHD · UNIVERSITY OF ILLINOIS AT CHICAGO · PI HARIJITH, ANANTHA · 2018 to 2022
$1.5M
American Heart Association 18TPA34230095Eunice Kennedy Shriver National Institute of Child Health and Human Development R01HD090887NICHD NIH HHS R01 HD090887
6 · The paper itself

Abstract

Premature infants are born with developing lungs burdened by surfactant deficiency and a dearth of antioxidant defense systems. Survival rate of such infants has significantly improved due to advances in care involving mechanical ventilation and oxygen supplementation. However, a significant subset of such survivors develops the chronic lung disease, Bronchopulmonary dysplasia (BPD), characterized by enlarged, simplified alveoli and deformed airways. Among a host of factors contributing to the pathogenesis is oxidative damage induced by exposure of the developing lungs to hyperoxia. Recent data indicate that hyperoxia induces aberrant sphingolipid signaling, leading to mitochondrial dysfunction and abnormal reactive oxygen species (ROS) formation (ROS). The role of sphingolipids such as ceramides and sphingosine 1-phosphate (S1P), in the development of BPD emerged in the last decade. Both ceramide and S1P are elevated in tracheal aspirates of premature infants of <32 weeks gestational age developing BPD. This was faithfully reflected in the murine models of hyperoxia and BPD, where there is an increased expression of sphingolipid metabolites both in lung tissue and bronchoalveolar lavage. Treatment of neonatal pups with a sphingosine kinase1 specific inhibitor, PF543, resulted in protection against BPD as neonates, accompanied by improved lung function and reduced airway remodeling as adults. This was accompanied by reduced mitochondrial ROS formation. S1P receptor1 induced by hyperoxia also aggravates BPD, revealing another potential druggable target in this pathway for BPD. In this review we aim to provide a detailed description on the role played by sphingolipid signaling in hyperoxia induced lung injury and BPD.

Indexed as

Airway RemodelingAnimalsAnimals, NewbornBronchopulmonary DysplasiaCeramidesDisease Models, AnimalHumansHyperoxiaInfantInfant, NewbornLungLung InjuryLysophospholipidsMethanolMiceOxidative StressCeramidesLysophospholipidsMethanolPF-543PyrrolidinesReactive Oxygen SpeciesSphingolipidsSphingosinesphingosine 1-phosphateSulfonesbronchopulmonary dysplasiaceramidemitochondrial dysfunctionROSS1Psphingolipid signaling

Identifiers

PMID35163176
PMCPMC8835774
OpenAlexW4207048037

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.