Evidence map›Paper›PMID 33733641›Full record

ArticleAllergy, asthma & immunology research2021

ATP6V0d2 Suppresses Alveoli Macrophage Alternative Polarization and Allergic Asthma via Degradation of PU.1.

Na Liu, Yuchen Feng, Huicheng Liu, Wenliang Wu, Yuxia Liang, Pingfei Li, Zhengping Wei, Min Wu, Zhao Hui Tang, Junyan Han and 6 more

Open access · diamondAbstract read
In one paragraph

Article in Allergy, asthma & immunology research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

8 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. SPI1Journal for immunotherapy of cancer · 2024
    Article
  6. Article
  7. Review
  8. 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

16 authors at 6 institutions in 3 countries.

Na Liu *Department of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan, China.ORCID https://orcid.org/0000-0001-9903-1314
Yuchen Feng *Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan, China.
Huicheng LiuDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan, China.
Wenliang WuDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan, China.
Yuxia LiangDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan, China.
Pingfei LiDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan, China.
Zhengping WeiDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan, China.
Min WuDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan, China.
Zhao Hui TangDepartment of Surgery, Tongji Hospital, Huazhong University of Science and Technology (HUST), Wuhan, China.
Junyan HanDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan, China.
Xiang ChengLaboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan, China.
Zheng LiuDepartment of Otolaryngology-Head and Neck Surgery, Tongji Hospital, Tongji Medical School, Huazhong University of Science and Technology (HUST), Wuhan, China.
Arian LaurenceUniversity College Hospital, NHS Trust, London, United Kingdom.ORCID https://orcid.org/0000-0003-0942-8292
Huabin LiDepartment of Otolaryngology, Head and Neck Surgery, Affiliated Eye-Ear-Nose and Throat Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0002-9837-2405
Guohua ZhenDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan, China.ORCID https://orcid.org/0000-0001-5582-7900
Xiang Ping YangDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan, China.ORCID https://orcid.org/0000-0001-9003-1772
Tongji Hospital · CNHuazhong University of Science and Technology · CNEye & ENT Hospital of Fudan University · CNHuazhong University of Science and Technology Hospital · CNUniversity College Hospital · GBWuhan Union Hospital · CN

Funding

Ministry of Science and Technology of the People's Republic of China 2019YFC1316203National Natural Science Foundation of China 31870892National Natural Science Foundation of China 81670019National Natural Science Foundation of China 81671539National Natural Science Foundation of China 81725004National Natural Science Foundation of China 91742108
6 · The paper itself

Abstract

purposeMacrophages are important regulators of environmental allergen-induced airway inflammation and asthma. ATP6V0d2 is a subunit of vacuolar ATPase highly expressed in macrophages. However, the functions of ATP6V0d2 in the regulation of pathogenesis of allergic asthma remain unclear. The aim of this study is to determine the function and related molecular mechanisms of macrophage protein ATP6V0d2 in allergic asthma.

methodsWe compared the disease severity between female C57BL/6 wild-type and

resultsThe expression of

conclusionsOur results identify macrophage Atp6v0d2, as an induced feedback inhibitor of asthma disease severity by promoting Pu.1 lysosomal degradation, which may in turn leads to reduced AAM polarization and Ccl17 production.

Indexed as

alveolar macrophageAsthmaPu.1 proteinV-type ATPase

Identifiers

PMID33733641
PMCPMC7984956
OpenAlexW3110319561

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.