Evidence map›Paper›PMID 32793225›Full record

ArticleFrontiers in immunology2020

Alveolar Epithelial Cells Promote IGF-1 Production by Alveolar Macrophages Through TGF-β to Suppress Endogenous Inflammatory Signals.

Mimi Mu, Peiyu Gao, Qian Yang, Jing He, Fengjiao Wu, Xue Han, Shujun Guo, Zhongqing Qian, Chuanwang Song

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

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  15. Mrc1Theranostics · 2024
    Article
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  19. Interaction between alveolar macrophages and epithelial cells duringFrontiers in cellular and infection microbiology · 2023
    Review
  20. 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

9 authors at 1 institution in 1 country.

Mimi MuDepartment of Immunology, School of Laboratory Medicine, Bengbu Medical College, Bengbu, China.
Peiyu GaoDepartment of Immunology, School of Laboratory Medicine, Bengbu Medical College, Bengbu, China.
Qian YangDepartment of Immunology, School of Laboratory Medicine, Bengbu Medical College, Bengbu, China.
Jing HeDepartment of Immunology, School of Laboratory Medicine, Bengbu Medical College, Bengbu, China.
Fengjiao WuDepartment of Immunology, School of Laboratory Medicine, Bengbu Medical College, Bengbu, China.
Xue HanDepartment of Immunology, School of Laboratory Medicine, Bengbu Medical College, Bengbu, China.
Shujun GuoDepartment of Immunology, School of Laboratory Medicine, Bengbu Medical College, Bengbu, China.
Zhongqing QianDepartment of Immunology, School of Laboratory Medicine, Bengbu Medical College, Bengbu, China.
Chuanwang SongDepartment of Immunology, School of Laboratory Medicine, Bengbu Medical College, Bengbu, China.
Bengbu Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To maintain alveolar gas exchange, the alveolar surface has to limit unnecessary inflammatory responses. This involves crosstalk between alveolar epithelial cells (AECs) and alveolar macrophages (AMs) in response to damaging factors. We recently showed that insulin-like growth factor (IGF)-1 regulates the phagocytosis of AECs. AMs secrete IGF-1 into the bronchoalveolar lavage fluid (BALF) in response to inflammatory stimuli. However, whether AECs regulate the production of IGF-1 by AMs in response to inflammatory signals remains unclear, as well as the role of IGF-1 in controlling the alveolar balance in the crosstalk between AMs and AECs under inflammatory conditions. In this study, we demonstrated that IGF-1 was upregulated in BALF and lung tissues of acute lung injury (ALI) mice, and that the increased IGF-1 was mainly derived from AMs.

Indexed as

Signal TransductionAlveolar Epithelial CellsAnimalsApoptosisCell CommunicationDisease Models, AnimalInsulin-Like Growth Factor ILipopolysaccharidesMacrophage ActivationMacrophages, AlveolarMicePhagocytosisPhosphatidylinositol 3-KinasesPneumoniaProto-Oncogene Proteins c-aktRNA InterferenceInsulin-Like Growth Factor ILipopolysaccharidesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTransforming Growth Factor betaAECAMsIGF-1inflammationTGF-β

Identifiers

PMID32793225
PMCPMC7385185
OpenAlexW3044032387

What OpenQuestion holds

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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.