ReviewEXCLI journal2026
Epigenetic regulation of PANoptosis: DNA methylation, histone modifications and non-coding RNAs.
Review in EXCLI journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Pyroptosis as a novel therapeutic target in glioblastoma multiforme: Mechanisms, molecular insights, and therapeutic potential.Molecular therapy. Nucleic acids · 2026Review
- Targeting the non-coding RNA-PANoptosis axis: a novel frontier in disease diagnosis and therapy.Apoptosis : an international journal on programmed cell death · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PANoptosome (Programmed Necrosis-Apoptosis Optosome) multiprotein complexes mediate the convergence of apoptosis, pyroptosis, and necroptosis. The ability of cells to undergo programmed inflammatory cell death is regulated by the epigenetic control of PANoptotic sensors, adaptors, and effectors, and has pivotal implications for their use in cancer therapies. DNA methylation suppresses the main PANoptotic pathways, such as RIPK3 (Receptor-Interacting Serine/Threonine-Protein Kinase 3), GSDME (Gasdermin E), and CASP8 (Caspase-8) that promote chemoresistance; hypomethylating DNA silencers resume PANoptotic sensitivity. BRD4 (Bromodomain-Containing Protein 4)/p300 (E1A-Associated Protein p300 - Histone Acetyltransferase) -mediated histone acetylation in enhancers (H3K27ac) stimulates ZBP1 (Z-DNA Binding Protein 1), NLRP3 (NOD-Like Receptor Family Pyrin Domain Containing 3), and caspase-8 transcription but inhibits the formation of inflammasomes by HDAC (Histone Deacetylase). PANoptotic regulatory regions become accessible in response to inflammatory signals through the dynamic regulation of accessibility through the SWI/SNF (Switch/Sucrose Non-Fermentable Chromatin Remodeling Complex) and NuRD (Nucleosome Remodeling Complex) and NuRD (Nucleosome Remodeling and Deacetylase Complex) chromatin remodelling complexes. Post-transcriptional regulation is mediated by ncRNAs (ncRNAs) such as miR-223-3p (MicroRNA-223-3p) and lncRNA NEAT1 (Long Non-Coding RNA - Nuclear Enriched Abundant Transcript 1) which converge to regulate the expression of NLRP3, RIPK3, and Gasdermin D (GSDMD). The interaction of DNA methylation, histone modification, and ncRNAs creates quantitative epigenetic thresholds that regulate PANoptotic sensitivity. The rational next step to overcome tumor immunoresistance is epigenetic biomarker stratification in combination with DNA methyltransferase inhibitors (DNMTi), histone deacetylase modulators (HDACi), and PANoptosis agonists, which could help reduce collateral tissue toxicity. See also the graphical abstract(Fig. 1).
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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 Socratic graph.