Evidence map›Paper›PMID 40025162›Full record

ArticleCommunications biology2025

Integrated transcriptomic profiling reveals a STING-mediated Type II Interferon signature in SOD1-mutant amyotrophic lateral sclerosis models.

Jen Young Hiew, Yi Shan Lim, Huitao Liu, Chen Seng Ng

Abstract read
In one paragraph

Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. LINE-1 Retrotransposons and Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026
    Review
  6. Expanding roles of cGAS-STING signaling in neuroinflammation.The Journal of clinical investigation · 2026
    Review
  7. Cellular Senescence of Patient-derived Fibroblasts Reveals the Mid-old Stage as a Critical Window for Transcriptomic Signatures Linked to Alzheimer's Disease Biomarkers and Classification.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026
    Article
  8. Review
  9. Review
  10. Article
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

4 authors.

Jen Young HiewSchool of Science, Monash University Malaysia, Jalan Lagoon Selatan, 47500, Selangor, Malaysia.
Yi Shan LimSchool of Science, Monash University Malaysia, Jalan Lagoon Selatan, 47500, Selangor, Malaysia.
Huitao LiuSchool of Biological Engineering, College of Advanced Interdisciplinary Science and Technology, Henan University of Technology, 100 Lianhua Street, Zhongyuan District, Zhengzhou, 450001, China.
Chen Seng NgSchool of Science, Monash University Malaysia, Jalan Lagoon Selatan, 47500, Selangor, Malaysia. ng.chenseng@monash.edu.ORCID http://orcid.org/0000-0002-3169-5795

Funding

International Brain Research Organization (IBRO) #PM010CNI000148Monash University Malaysia (Monash Malaysia) #SED000125
6 · The paper itself

Abstract

Inflammation is a hallmark of amyotrophic lateral sclerosis (ALS), particularly in cases with SOD1 mutations. Using integrative transcriptomics, we analyzed gene expression changes in mouse models throughout progression, human induced-pluripotent stem cells (hiPSCs), and post-mortem spinal cord tissue from ALS patients. We identified a conserved upregulation of interferon (IFN) genes and IFN-stimulating genes (ISGs) in both mouse models and human ALS, with a predominance Type I IFNs (IFN-α/β) in mice and Type II IFNs (IFN-γ) in humans. In mouse models, we observed robust and sustained upregulation of Type I and II ISGs, including ATF3, beginning at disease onset stage and persisting throughout disease progression. Single-cell transcriptomics further pinpointed vascular endothelial cells as a major source of ISGs. Furthermore, we found that the STING-TBK1 axis is essential for the induction of Type II ISGs in ALS, as its deletion impaired their expression. Our study uncovers a conserved ISGs signature across ALS models and patients, highlighting the potential role of innate immune activation in ALS pathogenesis. These findings suggest that ISGs may serve as potential biomarkers and therapeutic targets for ALS.

Indexed as

Amyotrophic Lateral SclerosisInterferon-gammaMembrane ProteinsMutationSuperoxide Dismutase-1TranscriptomeAnimalsDisease Models, AnimalFemaleGene Expression ProfilingHumansInduced Pluripotent Stem CellsMaleMiceSTING ProteinInterferon-gammaMembrane ProteinsSOD1 protein, humanSod1 protein, mouseSTING1 protein, humanSting1 protein, mouseSTING ProteinSuperoxide Dismutase-1

Identifiers

PMID40025162
PMCPMC11873215

What Socratic 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 Socratic graph.