ArticleNature communications2026
Arachidonic acid induces pyroptosis via a non-autophagic function of mitophagy and enhances immunotherapy in a PDAC model.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Integrated microbiome-metabolome analysis implicates Acinetobacter guillouiae in arachidonic acid metabolic remodeling and endometrial cancer cell proliferation.Biology direct · 2026Article
- Mechanistic insights into how intrapancreatic fat deposition drives the development of acute pancreatitis.International journal of biological sciences · 2026Review
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Authors and funding
20 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) presents a therapeutic hurdle owing to its immunotherapy resistance and limited treatment options. Pyroptosis, a lytic inflammatory cell death pathway, holds promise for reversing immunosuppression in "cold" tumors, yet tumor-specific induction strategies remain unclear. Here, we employ a contrastive learning graph neural network to identify arachidonic acid (AA), an endogenous ω-6 polyunsaturated fatty acid, as a pan-cancer pyroptosis inducer operating through irreversible mitochondrial permeability transition inducing Caspase 3/GSDME activation. Crucially, a repurposed mitophagy machinery for non-autophagic functional scaffolding of Caspase 3/GSDME on autophagosomal membranes enables rapid pyroptotic execution. Pharmacological accumulation of autophagosomes amplifies AA-induced pyroptosis in PDAC organoids and patient-derived xenografts. Furthermore, AA-triggered pyroptosis, remodels immunosuppressive tumor microenvironments, boosting cytotoxic T cell infiltration and synergizing with anti-PD-1 therapy in immunocompetent models. Thus, our findings position AA as a candidate dual-function agent for pyroptosis-immune synergy, while autophagosome manipulation emerges as a strategy to potentiating strategy.
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Registered trials
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