Evidence map›Paper›PMID 39415037›Full record

ArticlePediatric research2025

Bronchopulmonary dysplasia demonstrates dysregulated autotaxin/lysophosphatidic acid signaling in a neonatal mouse model.

Alison W Ha, Tara Sudhadevi, Anjum Jafri, Cathy Mayer, Peter M MacFarlane, Viswanathan Natarajan, Anantha Harijith

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Article in Pediatric research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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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

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3 · Its place in the literature

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Alison W HaDepartment of Biochemistry and Molecular Genetics, University of Illinois, Chicago, IL, USA.
Tara SudhadeviDepartment of Pediatrics, School of Medicine, Case Western Reserve University, Cleveland, OH, USA.
Anjum JafriDepartment of Genetics and Genome Sciences, School of Medicine, Case Western Reserve University, Cleveland, OH, USA.
Cathy MayerDepartment of Pediatrics, School of Medicine, Case Western Reserve University, Cleveland, OH, USA.
Peter M MacFarlaneDepartment of Pediatrics, School of Medicine, Case Western Reserve University, Cleveland, OH, USA.
Viswanathan NatarajanDepartment of Pharmacology, University of Illinois, Chicago, IL, USA.
Anantha HarijithDepartment of Pediatrics, School of Medicine, Case Western Reserve University, Cleveland, OH, USA. axh775@case.edu.

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 18TPA34230095NICHD NIH HHS R01 HD090887
6 · The paper itself

Abstract

backgroundBronchopulmonary dysplasia (BPD) is a chronic lung disease affecting premature infants who require oxygen supplementation and ventilator therapy to support their underdeveloped lungs. Autotaxin (ATX), an enzyme that generates the bioactive phospholipid lysophosphatidic acid (LPA), which acts via G-protein coupled receptors, has been implicated in numerous pulmonary diseases. In this study, we explored the pathophysiological role of the ATX/LPA signaling pathway in BPD.

methodsNeonatal mice were exposed to normoxia or hyperoxia (85%) for 14 days from birth while being treated with vehicle, ATX inhibitor or LPA receptor 1 (LPA

resultsAnimals exposed to hyperoxia showed elevated expression of ATX, ATX activity, and LPA

conclusionHyperoxia increases the expression of ATX and LPA IMPACT: Exposure to hyperoxia increases the expression and activity of autotaxin (ATX), as well as expression of LPA receptor 1 (LPA

Indexed as

Bronchopulmonary DysplasiaLysophospholipidsPhosphoric Diester HydrolasesSignal TransductionAnimalsAnimals, NewbornDisease Models, AnimalExtracellular MatrixFibroblastsHumansHyperoxiaLungLysophospholipase DMiceMice, Inbred C57BLProtein-Lysine 6-Oxidaselysophosphatidic acidLysophospholipase DLysophospholipidsPhosphoric Diester HydrolasesProtein-Lysine 6-OxidaseReceptors, Lysophosphatidic Acid

Identifiers

What Socratic 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 Socratic graph.