Evidence map›Paper›PMID 34803691›Full record

ArticleFrontiers in pharmacology2021

CXCR7 Antagonism Reduces Acute Lung Injury Pathogenesis.

Laetitia Pouzol, Anna Sassi, Nadège Baumlin, Mélanie Tunis, Daniel S Strasser, François Lehembre, Marianne M Martinic

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

11 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  6. ISGylation of NF-κBp65 by SCFArteriosclerosis, thrombosis, and vascular biology · 2023
    Article
  7. CXCL12-CXCR4/CXCR7 Axis in Cancer: from Mechanisms to Clinical Applications.International journal of biological sciences · 2023
    Review
  8. Review
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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

7 authors at 1 institution in 1 country.

Laetitia PouzolIdorsia Pharmaceuticals Ltd., Allschwil, Switzerland.
Anna SassiIdorsia Pharmaceuticals Ltd., Allschwil, Switzerland.
Nadège BaumlinIdorsia Pharmaceuticals Ltd., Allschwil, Switzerland.
Mélanie TunisIdorsia Pharmaceuticals Ltd., Allschwil, Switzerland.
Daniel S StrasserIdorsia Pharmaceuticals Ltd., Allschwil, Switzerland.
François LehembreIdorsia Pharmaceuticals Ltd., Allschwil, Switzerland.
Marianne M MartinicIdorsia Pharmaceuticals Ltd., Allschwil, Switzerland.
Idorsia (Switzerland) · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of control in the trafficking of immune cells to the inflamed lung tissue contributes to the pathogenesis of life-threatening acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome (ARDS). Targeting CXCR7 has been proposed as a potential therapeutic approach to reduce pulmonary inflammation; however, its role and its crosstalk with the two chemokine receptors CXCR3 and CXCR4 via their shared ligands CXCL11 and CXCL12 is not yet completely understood. The present paper aimed to characterize the pathological role of the CXCR3/CXCR4/CXCR7 axis in a murine model of ALI. Lipopolysaccharide (LPS) inhalation in mice resulted in the development of key pathologic features of ALI/ARDS, including breathing dysfunctions, alteration in the alveolar capillary barrier, and lung inflammation. LPS inhalation induced immune cell infiltration into the bronchoalveolar space, including CXCR3

Indexed as

acute lung injuryacute respiratory distress syndromeCXCL11CXCL12CXCR3CXCR4CXCR7immunomodulation

Identifiers

PMID34803691
PMCPMC8602191
OpenAlexW3211348587

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.