Evidence map›Paper›PMID 34561985›Full record

ReviewCurrent neuropharmacology2022

cGAS-STING-mediated IFN-I Response in Host Defense and Neuroinflammatory Diseases.

Kai Chen, Chuan Lai, Ying Su, Wen Dai Bao, Liu Nan Yang, Ping-Ping Xu, Ling-Qiang Zhu

Open access · greenAbstract readReview
In one paragraph

Review in Current neuropharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 58 citations in OpenAlex.

  1. AA and Parkinson's Disease.Reviews of physiology, biochemistry and pharmacology · 2027
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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 at 4 institutions in 1 country.

Kai ChenDepartment of Pathophysiology, Key Lab of Neurological Disorder of Education Ministry, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PRC.
Chuan LaiDepartment of Pathophysiology, Key Lab of Neurological Disorder of Education Ministry, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PRC.
Ying SuDepartment of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Wen Dai BaoDepartment of Pathophysiology, Key Lab of Neurological Disorder of Education Ministry, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PRC.
Liu Nan YangDepartment of Pathophysiology, Key Lab of Neurological Disorder of Education Ministry, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PRC.
Ping-Ping XuEndoscopy Center, Wuhan Children\'s Hospital, Tongji Medical College, Huazhong University of Science and Technology, P.R China, 430015.
Ling-Qiang ZhuDepartment of Pathophysiology, Key Lab of Neurological Disorder of Education Ministry, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PRC.
Huazhong University of Science and Technology · CNUnion Hospital · CNWuhan Children's Hospital · CNWuhan No.1 Hospital · CN

Funding

Fundamental Research Funds for the Central Universities', HUST 2019KFYXKJC076Hubei Provincial Natural Science Foundation 2020CFB811National Natural Science Foundation of China 82030032, 32070960, 81961128005, 81829002, 81871108, 31721002
6 · The paper itself

Abstract

The presence of foreign or misplaced nucleic acids is a dangerous signal that triggers innate immune responses by activating cytosolic DNA sensor cyclic GMP-AMP synthase (cGAS) and binding to its downstream signaling effector stimulator of interferon genes (STING). Then the cGAS-STING pathway activation links nucleic acid-sensing to immune responses and pathogenic entities clearance. However, the overactivation of this signaling pathway leads to fatal immune disorders and contributes to the progression of many human inflammatory diseases. Therefore, optimal activation of this pathway is crucial for the elimination of invading pathogens and the maintenance of immune homeostasis. In this review, we will summarize its fundamental roles in initiating host defense against invading pathogens and discuss its pathogenic roles in multiple neuro-inflammatory diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS) and other neurodegenerative diseases.

Indexed as

Interferon Type IMembrane ProteinsNeuroinflammatory DiseasesNucleotidyltransferasesCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNAHumansImmunity, InnatecGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNAInterferon Type IMembrane ProteinsNucleotidyltransferasesADALScGASHDMSneuroinflammationPDSTING

Identifiers

PMID34561985
PMCPMC9413793
OpenAlexW3201416860

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.