Evidence map›Paper›PMID 37746070›Full record

ArticleFrontiers in medicine2023

Increased lipocalin-2 expression in pulmonary inflammation and fibrosis.

Apostolos Galaris, Dionysios Fanidis, Eliza Tsitoura, Paraskevi Kanellopoulou, Ilianna Barbayianni, Konstantinos Ntatsoulis, Katerina Touloumi, Sofia Gramenoudi, Theodoros Karampitsakos, Argyrios Tzouvelekis and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
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

10 citing papers in PubMed, 16 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

12 authors at 3 institutions in 1 country.

Apostolos GalarisInstitute for Fundamental Biomedical Research, Biomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Dionysios FanidisInstitute for Fundamental Biomedical Research, Biomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Eliza TsitouraDepartment of Respiratory Medicine, School of Medicine, University of Crete, Heraklion, Greece.
Paraskevi KanellopoulouInstitute for Fundamental Biomedical Research, Biomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Ilianna BarbayianniInstitute for Fundamental Biomedical Research, Biomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Konstantinos NtatsoulisInstitute for Fundamental Biomedical Research, Biomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Katerina TouloumiInstitute for Fundamental Biomedical Research, Biomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Sofia GramenoudiInstitute for Fundamental Biomedical Research, Biomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Theodoros KarampitsakosDepartment of Respiratory Medicine, School of Medicine, University of Patras, Patras, Greece.
Argyrios TzouvelekisDepartment of Respiratory Medicine, School of Medicine, University of Patras, Patras, Greece.
Katerina AntoniouDepartment of Respiratory Medicine, School of Medicine, University of Crete, Heraklion, Greece.
Vassilis AidinisInstitute for Fundamental Biomedical Research, Biomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Alexander Fleming Biomedical Sciences Research Center · GRUniversity of Crete · GRUniversity of Patras · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Idiopathic Pulmonary Fibrosis (IPF) is a chronic, progressive interstitial lung disease with dismal prognosis. The underlying pathogenic mechanisms are poorly understood, resulting in a lack of effective treatments. However, recurrent epithelial damage is considered critical for disease initiation and perpetuation, via the secretion of soluble factors that amplify inflammation and lead to fibroblast activation and exuberant deposition of ECM components. Lipocalin-2 (LCN2) is a neutrophil gelatinase-associated lipocalin (NGAL) that has been suggested as a biomarker of kidney damage. LCN2 has been reported to modulate innate immunity, including the recruitment of neutrophils, and to protect against bacterial infections by sequestering iron. Methods: Results and discussion: Increased

Indexed as

acute lung injurybleomycin (BLM)idiopathic pulmonary fibrosis (IPF)lipocalin-2 (LCN2)transcriptomics

Identifiers

PMID37746070
PMCPMC10513431
OpenAlexW4386515398

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.