Evidence map›Paper›PMID 39920718›Full record

ReviewBiology direct2025

cGAS-STING targeting offers therapy choice in lung diseases.

Yu Wang, Xuan Zhang, Weixue Wang, Yi Zhang, Joshua S Fleishman, Hongquan Wang

Abstract readReview
In one paragraph

Review in Biology direct, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Lactylation: a novel post-translational modification for cGAS-STING pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  3. Mitochondrial DNA as a driver of inflammation via the cGAS-STING pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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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

6 authors.

Yu Wang *Department of Geriatrics, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, 100049, China.
Xuan Zhang *Clinical Pharmacology Research Center, Peking Union Medical College Hospital, State Key Laboratory of Complex Severe and Rare Diseases, NMPA Key Laboratory for Clinical Research and Evaluation of Drug, Beijing Key Laboratory of Clinical PK & PD Investigation for Innovative Drugs, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100730, China.
Weixue WangDepartment of Geriatrics, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, 100049, China.
Yi ZhangDepartment of Geriatrics, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, 100049, China.
Joshua S FleishmanDepartment of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY, 11439, USA. joshua.fleishman18@my.stjohns.edu.
Hongquan WangDepartment of Geriatrics, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, 100049, China. whongquan@alu.fudan.edu.cn.

Funding

Science Foundation of AMHT (2024YK05)
6 · The paper itself

Abstract

Cyclic GMP/AMP (cGAMP) synthase (cGAS), along with the endoplasmic reticulum (ER)-associated stimulator of interferon genes (STING), are crucial elements of the type 1 interferon response. cGAS senses microbial DNA and self-DNA, labeling cGAS-STING as a crucial mechanism in autoimmunity, sterile inflammatory responses, and cellular senescence. However, chronic and aberrant activation of the cGAS-STING axis results in inflammatory and autoimmune diseases. cGAS-STING has emerged as a vital mechanism driving inflammation-related diseases, including lung diseases. Insights into the biology of the cGAS-STING pathway have enabled the discovery of small-molecule agents which have the potential to inhibit the cGAS-STING axis in lung diseases. In this review, we first outline the principal components of the cGAS-STING signaling cascade. Then, we discuss recent research that highlights general mechanisms by which cGAS-STING contributes to lung diseases. Then, we focus on summarizing a list of bioactive small-molecule compounds which inhibit the cGAS-STING pathway, reviewing their potential mechanisms.These review highlights a novel groundbreaking therapeutic possibilities through targeting cGAS-STING in lung diseases.

Indexed as

Lung DiseasesMembrane ProteinsNucleotidyltransferasesAnimalsCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseHumansSignal TransductionSTING ProteincGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseMembrane ProteinsNucleotidyltransferasesSTING1 protein, humanSTING ProteinAntagonistcGASLung diseasesSTING

Identifiers

PMID39920718
PMCPMC11806777

What OpenQuestion holds

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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.