Evidence map›Paper›PMID 40360774›Full record

ArticlePediatric research2026

Proteomic analysis identifying proteins relevant for treatment success following experimental neonatal inflammation-sensitized hypoxia-ischemia.

Hannah Burkard, Damjan Osredkar, Elke Maes, Maria E Bernis, Anna-Sophie Bremer, Margit Zweyer, Paul Dowling, Kay Ohlendieck, Marianne Thoresen, Hemmen Sabir

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Article in Pediatric research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
–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

1 citing paper in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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

10 authors.

Hannah BurkardDepartment of Neonatology and Pediatric Intensive Care, Children's Hospital, University of Bonn, 53127, Bonn, Germany.
Damjan OsredkarDepartment of Pediatric Neurology, University Children's Hospital, University Medical Centre Ljubljana, Ljubljana, Slovenia.
Elke MaesDepartment of Neonatology and Pediatric Intensive Care, Children's Hospital, University of Bonn, 53127, Bonn, Germany.
Maria E BernisDepartment of Neonatology and Pediatric Intensive Care, Children's Hospital, University of Bonn, 53127, Bonn, Germany.
Anna-Sophie BremerDepartment of Neonatology and Pediatric Intensive Care, Children's Hospital, University of Bonn, 53127, Bonn, Germany.
Margit ZweyerDepartment of Neonatology and Pediatric Intensive Care, Children's Hospital, University of Bonn, 53127, Bonn, Germany.
Paul DowlingDepartment of Biology, Maynooth University, National University of Ireland, W23 F2H6 Maynooth, Co, Kildare, Ireland.
Kay OhlendieckDepartment of Biology, Maynooth University, National University of Ireland, W23 F2H6 Maynooth, Co, Kildare, Ireland.
Marianne ThoresenDepartment of Physiology, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Hemmen SabirDepartment of Neonatology and Pediatric Intensive Care, Children's Hospital, University of Bonn, 53127, Bonn, Germany. hemmen.sabir@dzne.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUnderstanding the mechanisms of injury following neonatal hypoxic-ischemic encephalopathy (HIE) is a major goal in neonatal research. HIE can have severe effects on cognitive and motor development in newborns, including an increased risk of death. As the incidence is 10-20 times higher in low- and middle-income countries compared to developed countries, the interest in a therapy exists worldwide. Therapeutic hypothermia (HT) is the only effective treatment after HIE. However, TH is not universally effective, particularly in cases of inflammation-sensitized hypoxia-ischemia (HI); it provides limited benefit.

methodsTo identify proteins that may contribute to the reduced efficacy of HT in the case of pre-HI inflammation sensitization, the proteomic profiles of animals subjected to HI and HT combined with lipopolysaccharide (LPS) were analyzed via liquid chromatography mass spectrometry (LC-MS/MS).

resultsWe identified proteins that potentially support the efficacy of HT and those that prevent the success of the therapy in the neonatal rat model of inflammation-sensitized HI.

conclusionThis study represents a step forward in identifying proteins related to the efficacy of HT following inflammation-sensitized HI. IMPACT: Therapeutic hypothermia is the only available treatment for neonatal hypoxic-ischemic encephalopathy, but not effective in models of inflammation-sensitized hypoxic-ischemic brain injury. Using liquid chromatography mass spectrometry, we identified proteins possibly having an effect on the treatment success of therapeutic hypothermia following experimental inflammation-sensitized hypoxic-ischemic brain injury. This proteomic analysis reveals proteins as potential markers that could prevent or support the efficacy of therapeutic hypothermia in experimental neonatal inflammation-sensitized hypoxic-ischemic encephalopathy.

Indexed as

Hypothermia, InducedHypoxia-Ischemia, BrainInflammationProteomicsAnimalsAnimals, NewbornChromatography, LiquidDisease Models, AnimalLipopolysaccharidesRatsRats, Sprague-DawleyTandem Mass SpectrometryTreatment OutcomeLipopolysaccharides

Identifiers

PMID40360774
PMCPMC13102700

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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.