Evidence map›Paper›PMID 40828197›Full record

ReviewArchives of toxicology2025

Interplay of cGAS-STING and ferroptosis: crosstalk, molecular mechanisms, and therapeutic prospects.

Yumin Wang, Shuang Wu, Yitong Wang, Clara Xi Wang, Weihua Zheng, Xia Yun, Zhiji Wang, Junjing Zhang, Lida Du, Hongquan Wang

Erratum issuedAbstract readReview
PubMed Publisher
In one paragraph

Review in Archives of toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–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

9 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. cGAS-STING as a Neuroimmune Traffic Molecule: Unraveling Pathogenic Mechanisms and Therapeutic Potential in Neurological Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Yumin Wang *Department of Respiratory and Critical Care Medicine, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, 100049, China.
Shuang Wu *Department of Neurology, Zhongnan Hospital of Wuhan University, Wuhan, 430000, China.
Yitong Wang *Department of Geriatrics, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, 100049, China.
Clara Xi WangSchool of Arts and Sciences, University of Pennsylvania, Philadelphia, PA, 19103, USA.
Weihua ZhengDepartment of Hepato-Biliary Surgery, Department of Surgery, Hohhot First Hospital, Hohhot, 010030, China.
Xia YunTeaching Department, Hohhot First Hospital, Hohhot, 010030, China.
Zhiji WangDivision of Neurobiology, Johns Hopkins University, Baltimore, MD, 21205, USA.
Junjing Zhang *Department of Hepato-Biliary Surgery, Department of Surgery, Hohhot First Hospital, Hohhot, 010030, China. zhang.jj@vip.163.com.
Lida DuDivision of Neurobiology, Johns Hopkins University, Baltimore, MD, 21205, USA. ldu13@jh.edu.
Hongquan WangDepartment of Geriatrics, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, 100049, China. whongquan@alu.fudan.edu.cn.ORCID 0000-0002-5447-2017

Funding

Beijing Natural Science Foundation 7252174Natural Science Foundation of Inner Mongolia Autonomous Region 2025MS08029
6 · The paper itself

Abstract

The cGAS-STING pathway, a crucial cytosolic DNA sensor, initiates innate immune responses by detecting microbial and aberrant self-DNA. This evolutionarily conserved axis plays pivotal roles in autoimmune disorders, sterile inflammation, and cellular senescence. While transient activation confers protective immunity, dysregulated cGAS-STING signaling drives pathogenesis in inflammatory and autoimmune diseases. Emerging evidence reveals its functional convergence with diverse cell death modalities-notably ferroptosis, an iron-dependent regulated cell death driven by lipid peroxidation. Their dynamic interplay emerges as a key pathogenic mechanism across diseases, offering novel therapeutic opportunities. This review first outlines the core molecular architecture of cGAS-STING signaling and its disease roles. We then analyze the mechanisms and pathophysiological consequences of cGAS-STING-ferroptosis crosstalk in various disorders, followed by advances in therapeutic strategies targeting this interface. Finally, we discuss translational challenges and propose innovative solutions. By highlighting the therapeutic potential of pharmacologically modulating this nexus, we identify a promising treatment for diseases with inflammatory conditions.

Indexed as

FerroptosisMembrane ProteinsNucleotidyltransferasesAnimalsAutoimmune DiseasesCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseHumansImmunity, InnateInflammationSignal TransductionSTING ProteincGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseMembrane ProteinsNucleotidyltransferasesSTING1 protein, humanSTING ProteinAntagonistcGAS-STINGFerroptosisInhibitorInterplay

Identifiers

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.