Evidence map›Paper›PMID 38272877›Full record

ArticleNature communications2024

Longitudinal plasma proteomics reveals biomarkers of alveolar-capillary barrier disruption in critically ill COVID-19 patients.

Erik Duijvelaar, Jack Gisby, James E Peters, Harm Jan Bogaard, Jurjan Aman

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

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  11. Plasma Proteins Associated with COVID-19 Severity in Puerto Rico.International journal of molecular sciences · 2024
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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

5 authors at 2 institutions in 2 countries.

Erik DuijvelaarDepartment of Pulmonary Medicine, Amsterdam University Medical Centers, Amsterdam Cardiovascular Sciences, Amsterdam, The Netherlands. e.duijvelaar@amsterdamumc.nl.ORCID 0000-0002-5547-5578
Jack GisbyDepartment of Immunology and Inflammation, Centre for Inflammatory Disease, Imperial College London, London, UK.ORCID 0000-0003-0511-8123
James E PetersDepartment of Immunology and Inflammation, Centre for Inflammatory Disease, Imperial College London, London, UK.ORCID 0000-0002-9415-3440
Harm Jan BogaardDepartment of Pulmonary Medicine, Amsterdam University Medical Centers, Amsterdam Cardiovascular Sciences, Amsterdam, The Netherlands.ORCID 0000-0001-5371-0346
Jurjan AmanDepartment of Pulmonary Medicine, Amsterdam University Medical Centers, Amsterdam Cardiovascular Sciences, Amsterdam, The Netherlands. j.aman@amsterdamumc.nl.ORCID 0000-0001-6211-1791
Amsterdam University Medical Centers · NLImperial College London · GB

Funding

Innovative Medicines Initiative (IMI) 101005142ZonMw (Netherlands Organisation for Health Research and Development) 10430 01 201 0007
6 · The paper itself

Abstract

The pathobiology of respiratory failure in COVID-19 consists of a complex interplay between viral cytopathic effects and a dysregulated host immune response. In critically ill patients, imatinib treatment demonstrated potential for reducing invasive ventilation duration and mortality. Here, we perform longitudinal profiling of 6385 plasma proteins in 318 hospitalised patients to investigate the biological processes involved in critical COVID-19, and assess the effects of imatinib treatment. Nine proteins measured at hospital admission accurately predict critical illness development. Next to dysregulation of inflammation, critical illness is characterised by pathways involving cellular adhesion, extracellular matrix turnover and tissue remodelling. Imatinib treatment attenuates protein perturbations associated with inflammation and extracellular matrix turnover. These proteomic alterations are contextualised using external pulmonary RNA-sequencing data of deceased COVID-19 patients and imatinib-treated Syrian hamsters. Together, we show that alveolar capillary barrier disruption in critical COVID-19 is reflected in the plasma proteome, and is attenuated with imatinib treatment. This study comprises a secondary analysis of both clinical data and plasma samples derived from a clinical trial that was registered with the EU Clinical Trials Register (EudraCT 2020-001236-10, https://www.clinicaltrialsregister.eu/ctr-search/trial/2020-001236-10/NL ) and Netherlands Trial Register (NL8491, https://www.trialregister.nl/trial/8491 ).

Indexed as

COVID-19BiomarkersCritical IllnessHumansImatinib MesylateInflammationProteomicsSARS-CoV-2BiomarkersImatinib Mesylate

Identifiers

PMID38272877
PMCPMC10811341
OpenAlexW4391230815

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.