Evidence map›Paper›PMID 35098856›Full record

ArticleAutophagy2022

Involvement of autophagy in exacerbation of eosinophilic airway inflammation in a murine model of obese asthma.

Yuzo Suzuki, Yuya Aono, Norimichi Akiyama, Yasuoki Horiike, Hyogo Naoi, Ryo Horiguchi, Kiyoshi Shibata, Hironao Hozumi, Masato Karayama, Kazuki Furuhashi and 5 more

Open access · greenAbstract read
In one paragraph

Article in Autophagy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

15 citing papers in PubMed, 34 citations in OpenAlex.

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  4. Serum autophagy protein 5 is positively related to T helper 2/T helper 1 ratio, inflammation, and exacerbation in adult asthma patients.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 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

15 authors at 1 institution in 1 country.

Yuzo SuzukiSecond Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.ORCID 0000-0001-6154-9791
Yuya AonoSecond Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Norimichi AkiyamaSecond Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Yasuoki HoriikeSecond Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Hyogo NaoiSecond Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Ryo HoriguchiAdvanced Research Facilities and Services, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Kiyoshi ShibataAdvanced Research Facilities and Services, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Hironao HozumiSecond Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Masato KarayamaSecond Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Kazuki FuruhashiSecond Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Noriyuki EnomotoSecond Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Tomoyuki FujisawaSecond Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Yutaro NakamuraSecond Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Naoki InuiSecond Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Takafumi SudaSecond Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Hamamatsu University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity is a common comorbidity in patients with asthma, and obese asthma patients present the most refractory phenotype among patients with severe asthma. Similar to the observations in non-obese asthma patients, clinical studies have revealed heterogeneity in obese asthma patients, including the occurrences of T helper (Th)2-high and Th2-low phenotypes. However, the mechanisms underlying obesity-related asthma are not completely understood. Though macroautophagy/autophagy is involved in asthma and obesity, its role in obesity-associated asthma is unknown. We hypothesized that autophagy is involved in the pathogenesis of obese asthma. For our investigations, we used high-fat diet-induced

Indexed as

AsthmaInterleukin-33AnimalsAutophagyCytokinesDisease Models, AnimalInflammationLungMiceObesityPyroglyphidaeCytokinesInterleukin-33Asthmaautophagycorticosteroid resistanceeosinophil inflammationIL33obesitythymic stromal lymphopoietin

Identifiers

PMID35098856
PMCPMC9397451
OpenAlexW4210381020

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.