Evidence map›Paper›PMID 36465073›Full record

ReviewRheumatology and immunology research2021

Regulation of cGAS-STING Pathway - Implications for Systemic Lupus Erythematosus.

Audrey M Hagiwara, Richard E Moore, Daniel J Wallace, Mariko Ishimori, Caroline A Jefferies

Open access · diamondAbstract readReview
In one paragraph

Review in Rheumatology and immunology research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Audrey M HagiwaraDivision of Rheumatology, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, CA, USA.
Richard E MooreDivision of Rheumatology, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, CA, USA.
Daniel J WallaceDivision of Rheumatology, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, CA, USA.
Mariko IshimoriDivision of Rheumatology, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, CA, USA.
Caroline A JefferiesDivision of Rheumatology, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, CA, USA.
Cedars-Sinai Medical Center · USUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type I interferon (IFN-I) is implicated in the pathogenesis of systemic lupus erythematosus (SLE) and the closely associated monogenic autoinflammatory disorders termed the "interferonopathies." Recently, the cytosolic DNA sensor cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS) and its downstream signaling adaptor stimulator of interferon genes (STING) have been identified as having important, if not central, roles in driving IFN-I expression in response to self-DNA. This review highlights the many ways in which this pathway is regulated in order to prevent self-DNA recognition and underlines the importance of maintaining tight control in order to prevent autoimmune disease. We will discuss the murine and human studies that have implicated the cGAS-STING pathway as being an important contributor to breakdown in tolerance in SLE and highlight the potential therapeutic application of this knowledge for the treatment of SLE.

Indexed as

cGASSTINGsystemic lupus erythematosustype I interferon

Identifiers

PMID36465073
PMCPMC9524788
OpenAlexW4200535965

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.