Evidence map›Paper›PMID 35222397›Full record

ArticleFrontiers in immunology2022

P2Y1R Ligation Suppresses Th17 Cell Differentiation and Alleviates Colonic Inflammation in an AMPK-Dependent Manner.

Yao-Yao Chang, Qiu-Chan Huan, Jiao Peng, Wen-Chun Bi, Li-Xiang Zhai, Yan Chen, Jonathan R Lamb, Xiang-Chun Shen, Zhao-Xiang Bian, Hai-Qiang Wu and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Activation of P2Y1R impedes intestinal mucosa repair during colitis.International journal of biological sciences · 2023
    Article
  5. The Role of AMPK Signaling in Ulcerative Colitis.Drug design, development and therapy · 2023
    Review
  6. 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

12 authors at 6 institutions in 3 countries.

Yao-Yao ChangSchool of Pharmaceutical Sciences, Health Science Center, Shenzhen University, Shenzhen, China.
Qiu-Chan HuanThe State Key Laboratory of Functions and Applications of Medicinal Plants and The High Efficacy Application of Natural Medicinal Resources Engineering Center of Guizhou Province, School of Pharmaceutical Sciences, Guizhou Medical University, Guizhou, China.
Jiao PengDepartment of Pharmacy, Peking University Shenzhen Hospital, Shenzhen, China.
Wen-Chun BiSchool of Pharmaceutical Sciences, Health Science Center, Shenzhen University, Shenzhen, China.
Li-Xiang ZhaiSchool of Chinese Medicine, Hong Kong Baptist University, Kowloon, Hong Kong SAR, China.
Yan ChenDepartment of Surgery, The University of Hong Kong, Hong Kong, Hong Kong SAR, China.
Jonathan R LambDepartment of Life Sciences, Faculty of Natural Sciences, Imperial College London, London, United Kingdom.
Xiang-Chun ShenThe State Key Laboratory of Functions and Applications of Medicinal Plants and The High Efficacy Application of Natural Medicinal Resources Engineering Center of Guizhou Province, School of Pharmaceutical Sciences, Guizhou Medical University, Guizhou, China.
Zhao-Xiang BianSchool of Chinese Medicine, Hong Kong Baptist University, Kowloon, Hong Kong SAR, China.
Hai-Qiang WuSchool of Pharmaceutical Sciences, Health Science Center, Shenzhen University, Shenzhen, China.
Yong-Xian ChengSchool of Pharmaceutical Sciences, Health Science Center, Shenzhen University, Shenzhen, China.
Hai-Tao XiaoSchool of Pharmaceutical Sciences, Health Science Center, Shenzhen University, Shenzhen, China.
Shenzhen University Health Science Center · CNHong Kong Baptist University · HKPeking University Shenzhen Hospital · CNGuiyang Medical University · CNImperial College London · GBUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

P2Y1 receptor is a G-protein-coupled receptor that plays a critical role in the immune response of inflammatory bowel diseases. However, its regulatory effects on CD4

Indexed as

ColitisNuclear Receptor Subfamily 1, Group F, Member 3AMP-Activated Protein KinasesAnimalsCell DifferentiationInflammationInterleukin-17MiceTh17 CellsAMP-Activated Protein KinasesInterleukin-17Nuclear Receptor Subfamily 1, Group F, Member 3AMPKcolitisdifferentiationP2Y1RTh17 cell

Identifiers

PMID35222397
PMCPMC8866175
OpenAlexW4211246816

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.