Evidence map›Paper›PMID 35764553›Full record

ReviewZhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology2022

[Activation of cGAS/STING signaling pathway and its immunological role in the progression of nonalcoholic fatty liver disease].

C X Sha, L L Ju, P Zhou, D F Yao, Min Yao

Open access · greenAbstract readReview
In one paragraph

Review in Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 61% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

5 authors at 2 institutions in 1 country.

C X ShaDepartment of Immunology, Medical School of Nantong University, Nantong 226001, China.
L L JuDepartment of Immunology, Medical School of Nantong University, Nantong 226001, China.
P ZhouDepartment of Immunology, Medical School of Nantong University, Nantong 226001, China.
D F YaoResearch Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong 226001, China.
Min YaoDepartment of Immunology, Medical School of Nantong University, Nantong 226001, China.
Nantong University · CNAffiliated Hospital of Nantong University · CN

Funding

Basic Medical Key Project of Nantong S.&T. Program of China MS12020021National Natural Science Foundation 31872738
6 · The paper itself

Abstract

Today, nonalcoholic fatty liver disease remains the most dominant chronic liver disease. Cyclic guanosine monophosphate-adenosine monosphosphate synthase (cGAS) is a cytosolic DNA sensor that catalyzes the synthesis of cyclic guanosine monophosphate, activates stimulator of interferon genes (STING), and releases type-I interferon cytokines to trigger immune responses. Exogenous or endogenous DNA acts as a cGAS ligand to activate the cGAS-STING signaling pathway, which plays a role in hepatitis, nonalcoholic fatty liver disease, liver cancer and other diseases, and affects liver disease progression and metabolism through mechanisms such as autophagy. This article reviews the activation of cGAS-STING pathway and its molecular immunological role in nonalcoholic fatty liver disease progression.

Indexed as

Interferon Type INon-alcoholic Fatty Liver DiseaseGuanosine MonophosphateHumansMembrane ProteinsNucleotidyltransferasesSignal TransductionGuanosine MonophosphateInterferon Type IMembrane ProteinsNucleotidyltransferases

Identifiers

PMID35764553
PMCPMC12770785
OpenAlexW4283726902

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.