Evidence map›Paper›PMID 33125041›Full record

ArticleEndocrinology2020

GLP-1 Receptor Signaling Differentially Modifies the Outcomes of Sterile vs Viral Pulmonary Inflammation in Male Mice.

Takehiro Sato, Tatsunori Shimizu, Hiroki Fujita, Yumiko Imai, Daniel J Drucker, Yutaka Seino, Yuichiro Yamada

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 26 citations in OpenAlex.

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  17. Liraglutide pretreatment attenuates sepsis-induced acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2023
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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 4 institutions in 2 countries.

Takehiro SatoDepartment of Endocrinology, Diabetes, and Geriatric Medicine, Akita University Graduate School of Medicine, Akita, Japan.
Tatsunori ShimizuDepartment of Endocrinology, Diabetes, and Geriatric Medicine, Akita University Graduate School of Medicine, Akita, Japan.
Hiroki FujitaDepartment of Endocrinology, Diabetes, and Geriatric Medicine, Akita University Graduate School of Medicine, Akita, Japan.
Yumiko ImaiLaboratory of Regulation for Intractable Infectious Diseases, Center for Vaccine and Adjuvant Research, National Institutes of Biomedical Innovation Health and Nutrition, Osaka, Japan.
Daniel J DruckerDepartment of Medicine, Lunenfeld-Tanenbaum Research Institute, Mt. Sinai Hospital, University of Toronto, Toronto, Canada.
Yutaka SeinoKansai Electric Power Medical Research Institute, Osaka, Japan.
Yuichiro YamadaDepartment of Endocrinology, Diabetes, and Geriatric Medicine, Akita University Graduate School of Medicine, Akita, Japan.
Akita University · JPKansai Electric Power (Japan) · JPNational Institute of Biomedical Innovation, Health and Nutrition · JPUniversity of Toronto · CA

Funding

CIHR 154321
6 · The paper itself

Abstract

A number of disease states, including type 2 diabetes (T2D), are associated with an increased risk of pulmonary infection. Glucagon-like peptide-1 (GLP-1) receptor agonists are used to treat T2D and exert anti-inflammatory actions through a single, well-defined GLP-1 receptor (GLP-1R). Although highly expressed in the lung, little is known about the role of the GLP-1R in the context of pulmonary inflammation. Here we examined the consequences of gain or loss of GLP-1R activity in infectious and noninfectious lung inflammation. We studied wild-type mice treated with a GLP-1R agonist, and Glp1r-/- mice, in the setting of bleomycin-induced noninfectious lung injury and influenza virus infection. Loss of the GLP-1R attenuated the severity of bleomycin-induced lung injury, whereas activation of GLP-1R signaling increased pulmonary inflammation via the sympathetic nervous system. In contrast, GLP-1R agonism reduced the pathogen load in mice with experimental influenza virus infection in association with increased expression of intracellular interferon-inducible GTPases. Notably, the GLP-1 receptor agonist liraglutide improved the survival rate after influenza virus infection. Our results reveal context-dependent roles for the GLP-1 system in the response to lung injury. Notably, the therapeutic response of GLP-1R agonism in the setting of experimental influenza virus infection may have relevance for ongoing studies of GLP-1R agonism in people with T2D susceptible to viral lung injury.

Indexed as

AnimalsBleomycinGlucagon-Like Peptide-1 ReceptorGlucagon-Like Peptide-1 Receptor AgonistsIncretinsLiraglutideMaleMiceMice, KnockoutOrthomyxoviridae InfectionsPneumoniaSignal TransductionBleomycinGlucagon-Like Peptide-1 ReceptorGlucagon-Like Peptide-1 Receptor AgonistsIncretinsLiraglutideglucagon-like peptide-1 (GLP-1)influenzalung inflammation

Identifiers

PMID33125041
PMCPMC7678414
OpenAlexW3096077207

What OpenQuestion 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 OpenQuestion graph.