ReviewJournal of translational medicine2025
Inflammatory mitochondrial signalling and viral mimicry in cancer.
Review in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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.
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Who cites it
8 citing papers in PubMed.
- The cGAS-STING pathway: mechanistic basis, dual biological functions and translational therapeutic advances.Apoptosis : an international journal on programmed cell death · 2026Review
- Quercetin induces molecular hallmarks of immunogenic cell death and cGAS-STING pathway activation via mitochondrial DNA release in hepatocellular carcinoma cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Quantitative Control of Transposable Elements: From Genome Plasticity to Immune Regulatory Circuits.Cell biochemistry and function · 2026Review
- Retrotransposons in Bone and Joint Diseases.FASEB bioAdvances · 2026Review
- Mitochondrial Dysfunction in the Inflammatory Process of Neurodegenerative Diseases.Biomedicines · 2026Review
- Single-Cell RNA-Seq Profiling of Transposable Element Expression in Human Peripheral Blood Cells During Viral Infections.International journal of molecular sciences · 2026Article
- Mitochondrial dysfunction acts as a modulator of the immunometabolic route for activating the cytosolic DNA sensor pathway in triggering innate immunosurveillance.Journal of translational medicine · 2025Review
- Mitochondrial signalling pathways in inflammation and health: mechanistic insights of mitochondrial impairment on cellular homeostasis in driving pathogenesis.Journal of translational medicine · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endogenous transposable elements (TEs) are receiving increasing attention as potential targets to develop novel immunostimulatory strategies against cancer. Indeed, the defective epigenetic suppression of TEs in malignant cells offers a therapeutic window to enable their re-activation with at least some degree of selectivity. In line with this notion, multiple clinically employed epigenetic modifiers such as DNA-demethylating agents have been shown to promote the re-expression of TEs in preclinical tumour models, hence driving powerful inflammatory responses that enables increased sensitivity of immunitary immune cells to immunotherapy with immune checkpoint inhibitors (ICIs). This phenomenon is commonly referred to as "viral mimicry" as (at least in part) it impinges on the activation of immunological pathways commonly driven by viral infection, notably the detection of cytosolic nucleic acids by pattern recognition receptors. Here, we critically discuss the molecular mechanisms through which the mitochondria-dependent cGAS-STING and MAVS pathways enable viral mimicry as elicited by the re-activation of TEs in neoplastic cells, as we comment on the therapeutic potential of using epigenetic modifiers to harness these mechanisms in support of restored ICIs sensitivity across cancer types.
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Registered trials
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.