Evidence map›Paper›PMID 37181813›Full record

ReviewMediators of inflammation2023

The Role of Macrophage Autophagy in Asthma: A Novel Therapeutic Strategy.

Lijie Wang, Xingxing Yuan, Zhuying Li, Fumin Zhi

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 17% 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

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
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

4 authors at 2 institutions in 1 country.

Lijie WangDepartment of Respiratory Medicine, The First Affiliated Hospital, Heilongjiang University of Chinese Medicine, Harbin 150040, China.ORCID https://orcid.org/0009-0006-7381-3485
Xingxing YuanHeilongjiang University of Chinese Medicine, Harbin 150040, China.ORCID https://orcid.org/0000-0002-9894-4127
Zhuying LiDepartment of Respiratory Medicine, The First Affiliated Hospital, Heilongjiang University of Chinese Medicine, Harbin 150040, China.ORCID https://orcid.org/0009-0006-9282-2619
Fumin ZhiDepartment of Medical, The First Affiliated Hospital, Heilongjiang University of Chinese Medicine, Harbin 150040, China.ORCID https://orcid.org/0000-0002-9662-746X
First Affiliated Hospital of Heilongjiang University of Chinese Medicine · CNHeilongjiang University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma is a chronic respiratory disease frequently associated with airway inflammation and remodeling. The development of asthma involves various inflammatory phenotypes that impact therapeutic effects, and macrophages are master innate immune cells in the airway that exert diverse functions including phagocytosis, antigen presentation, and pathogen clearance, playing an important role in the pathogeneses of asthma. Recent studies have indicated that autophagy of macrophages affects polarization of phenotype and regulation of inflammation, which implies that regulating autophagy of macrophages may be a potential strategy for the treatment of asthma. Thus, this review summarizes the signaling pathways and effects of macrophage autophagy in asthma, which will provide a tactic for the development of novel targets for the treatment of this disease.

Indexed as

AsthmaAutophagyHumansInflammationMacrophagesPhagocytosis

Identifiers

PMID37181813
PMCPMC10175021
OpenAlexW4368617767

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.