Evidence map›Paper›PMID 39305055›Full record

ArticleClinical and translational medicine2024

IFIT3 mediates TBK1 phosphorylation to promote activation of pDCs and exacerbate systemic sclerosis in mice.

Xiangyang Huang, Yi Liu, Xia Rong, Yiheng Zhao, Dan Feng, Jun Wang, Wanhong Xing

Abstract read
In one paragraph

Article in Clinical and translational medicine, 2024. 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
–field-weighted citation impact
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.

  1. Pooled it
  2. Article
  3. Article
  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

7 authors.

Xiangyang HuangDepartment of Rheumatology and Immunology, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, China.ORCID 0000-0003-3255-5775
Yi LiuDepartment of Communication Sciences & Disorders, MGH Institute of Health Professions, Boston, Massachusetts, USA.
Xia RongDepartment of Rheumatology and Immunology, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, China.
Yiheng ZhaoDepartment of Rheumatology and Immunology, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, China.
Dan FengDepartment of Rheumatology and Immunology, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, China.
Jun WangDepartment of Rheumatology and Immunology, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, China.
Wanhong XingDepartment of Cardiothoracic Surgery, The Sixth People's Hospital of Chengdu, Chengdu, Sichuan, China.

Funding

National Natural Science Foundation of China 81871298
6 · The paper itself

Abstract

objectiveTo assess the impact of the IFIT3/TBK1 signalling pathway in activating plasmacytoid dendritic cells (pDCs) and its role in the development of SSc.

methodsUtilized single-cell RNA sequencing (scRNA-seq) and high-throughput transcriptome RNA sequencing to reveal the differential abundance of pDCs and the role of the key gene IFIT3 in SSc. Conducted in vitro cell experiments to evaluate the effect of IFIT3/TBK1 signalling pathway intervention on pDC activation cytokine release and fibroblast function. Constructed an IFIT3

resultsThe IFIT3/TBK1 signalling pathway plays a crucial role in activating pDCs, with IFIT3 acting as an upstream regulator of TBK1. Intervention in the IFIT3/TBK1 signalling pathway can inhibit pDC activation cytokine release and impact fibroblast function. The IFIT3

conclusionThis study provides new insights into potential therapeutic targets for SSc, highlighting the critical role of the IFIT3/TBK1 signalling pathway in SSc development. HIGHLIGHTS: This study elucidates the pivotal role of plasmacytoid dendritic cells (pDCs) in systemic sclerosis (SSc). This study identified the key regulatory gene involved in systemic sclerosis (SSc) as IFIT3. This study has found that IFIT3 functions as an upstream regulatory factor, activating TBK1. This study provides Evidence of the regulatory effects of the IFIT3/TBK1 pathway on plasmacytoid dendritic cells (pDCs). This study validated the therapeutic potential using the IFIT3

Indexed as

Dendritic CellsDisease Models, AnimalProtein Serine-Threonine KinasesScleroderma, SystemicAnimalsFemaleIntracellular Signaling Peptides and ProteinsMaleMiceMice, KnockoutPhosphorylationSignal TransductionIfit3 protein, mouseIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesTbk1 protein, mouseCRISPR/Cas9fibrosisIFIT3/TBK1 signalling pathwaypDCs activationscRNA‐seqsystemic sclerosis

Identifiers

PMID39305055
PMCPMC11415598

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.