Evidence map›Paper›PMID 34076707›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2021

FSTL1 aggravates OVA-induced inflammatory responses by activating the NLRP3/IL-1β signaling pathway in mice and macrophages.

Yan Wang, Dong Zhang, Tian Liu, Jun-Fei Wang, Jin-Xiang Wu, Ji-Ping Zhao, Jia-Wei Xu, Jin-Tao Zhang, Liang Dong

Abstract read
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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
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  4. Role of GLCCI1 in inhibiting PI3K-induced NLRP3 inflammasome activation in asthma.Chinese medical journal pulmonary and critical care medicine · 2024
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. IL-18 biology in severe asthma.Frontiers in medicine · 2024
    Review
  13. International journal of molecular sciences · 2023
    Article
  14. Article
  15. Review
  16. Review
  17. 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 2 institutions in 1 country.

Yan Wang *Department of Pulmonary Diseases, Qilu Hospital (Qingdao), Cheeloo College of Medicine, Shandong University, Qingdao, Shandong, People's Republic of China.
Dong Zhang *Department of Respiratory, Shandong Qianfoshan Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Tian LiuDepartment of Pulmonary Diseases, Qilu Hospital, Shandong University, Jinan, Shandong, People's Republic of China.
Jun-Fei WangDepartment of Pulmonary Diseases, Qilu Hospital, Shandong University, Jinan, Shandong, People's Republic of China.
Jin-Xiang WuDepartment of Pulmonary Diseases, Qilu Hospital, Shandong University, Jinan, Shandong, People's Republic of China.
Ji-Ping ZhaoDepartment of Pulmonary Diseases, Qilu Hospital, Shandong University, Jinan, Shandong, People's Republic of China.
Jia-Wei XuDepartment of Respiratory, Shandong Qianfoshan Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Jin-Tao ZhangDepartment of Respiratory, Shandong Qianfoshan Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Liang DongDepartment of Respiratory, Shandong Provincial Qianfoshan Hospital, Shandong University, The First Affiliated Hospital of Shandong First Medical University, Shandong Institute of Respiratory Diseases, Jinan, China. dl5506@126.com.ORCID http://orcid.org/0000-0001-7707-9982
Shandong University · CNQilu Hospital of Shandong University · CN

Funding

National Natural Science Foundation of China 81770029
6 · The paper itself

Abstract

objectiveAsthma, a well-known disease with high morbidity, is characterized by chronic airway inflammation. However, the allergic inflammation mechanisms of follistatin-like protein 1 (FSTL1) have not been elucidated. This study aims to investigate the effects of FSTL1 in ovalbumin (OVA)-induced mice and macrophages on nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3)/interleukin-1β (IL-1β) signaling pathway.

methodsMice were randomly divided into control-WT, OVA-WT, control-Fstl1

resultsThe present results uncovered that Fstl1

conclusionsThe study results showed that FSTL1 played an important role in allergic airway inflammation by activating NLRP3/IL-1β. Hence, inhibition FSTL1 could be applied as a therapeutic agent against asthma.

Indexed as

AgedAllergensAnimalsAsthmaBronchoalveolar Lavage FluidCell LineCytokinesFemaleFollistatin-Related ProteinsFuransHumansIndenesLungMacrophagesMaleMiceAllergensCytokinesFollistatin-Related ProteinsFuransIndenesN-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamideNLR Family, Pyrin Domain-Containing 3 ProteinOvalbuminSulfonamidesAirway inflammationAlveolar macrophage cellsAsthmaFSTL1IL-1βNLRP3

Identifiers

PMID34076707
OpenAlexW3164053816

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.