Pyroptosis
Pyroptosis is a form of regulated cell death characterized by inflammatory signaling, disruption of the plasma membrane, and release of intracellular danger signals.
Pyroptosis is a form of regulated cell death characterized by inflammatory signaling, disruption of the plasma membrane, and release of intracellular danger signals. It is commonly initiated by inflammasomes such as the NLRP3 inflammasome, which activate caspase-1. Caspase-1 cleaves Gasdermin D (GSDMD), releasing its pore-forming fragment and promoting cellular swelling, membrane rupture, and secretion of interleukin-1β (IL-1β) and interleukin-18 (IL-18). Pyroptosis can also be initiated through non-canonical inflammasome pathways, which respond to cytosolic lipopolysaccharide and activate inflammatory caspases that converge on GSDMD.
Additional pyroptotic routes involve apoptotic caspases and other gasdermins. For example, caspase-3 can cleave Gasdermin E (GSDME), thereby redirecting apoptotic signaling toward a pyroptosis-like, inflammatory form of cell death. Release of high mobility group box 1 (HMGB1), proinflammatory cytokines, and other damage-associated molecular patterns can amplify inflammation and influence macrophage activity, antigen presentation, and adaptive immune responses. In contrast with the generally immunologically quiet dismantling associated with apoptosis, pyroptosis is considered an immunogenic cell-death modality that can stimulate dendritic-cell and T-cell responses; it is therefore studied both as a driver of inflammatory disease and as a potential mechanism for cancer therapy.
Rebuilt from PubMed 9 Sept 2026 · no new papers today
Where the papers sit
11 papers study pyroptosis directly. The themes below are drawn from those 11.
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Inflammasome-Driven Tissue Injury : NLRP3–CASP1–GSDMD signaling recurs as a target for limiting inflammatory tissue injury in sepsis, diabetic liver disease, mastitis and peripheral nerve damage. Oxyphenbutazone, Tuolitounong decoction and aconitine are explored to suppress IL-1β-linked pyroptosis, with recovery or inflammatory protection as endpoints. 4 papers · 36.4%
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GSDME Cancer Immunotherapy : GSDME delivery and activation are being used to turn tumor killing into immune reprogramming, especially alongside radiotherapy. Biomimetic nanovesicles and a mitochondria-targeted iridium complex recur across glioblastoma and breast cancer, with dendritic-cell maturation and tumor-antigen release as endpoints. 3 papers · 27.3%
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Others — Programmed Cell Death Therapies : Programmed cell-death strategies range from proteasome-inhibitor-resistant myeloma and lung cancer to tissue-repair biomaterials. Pyroptosis, disulfidptosis and immunogenic cell death recur, but the applications do not establish a single therapeutic direction. 4 papers · 36.4%
Recent Findings on pyroptosis
Biomaterial-Driven Pyroptosis: Cur@ZIF-8/SIM@CACM inhibited BMSC pyroptosis through the NLRP3/Caspase-1/GSDMD pathway and improved hyaline cartilage-like regeneration 42576623Aug. Mito-Ir and QSSC@Exo-LNP instead deliberately amplified pyroptosis to treat cancer and stimulate immunogenic cell death 42489638Jul42466899Jul. Mito-Ir used mitochondrial dysfunction to activate the caspase-3/GSDME pathway, whereas QSSC@Exo-LNP combined caspase-8 activation with EGFR inhibition and caspase-3 amplification 42489638Jul42466899Jul. CuN3Cl-BAY@COD further paired pyroptosis with disulfidptosis, metabolic reprogramming, and hydrogen peroxide accumulation for prostate cancer immunotherapy 42424164Jul. These results are moving toward multifunctional platforms that select pyroptosis inhibition for tissue repair or pyroptosis induction for tumour killing and immune reprogramming.
Inflammasome-Mediated Tissue Injury: Aconitine, TNF-α inhibition, oxyphenbutazone, and Tuolitounong Decoction all reduced inflammasome-associated pyroptosis while improving inflammatory tissue injury 42480279Jul42219549May42150290May42142128May. Aconitine suppressed NLRP3 inflammasome activation through TLR4/MyD88/NF-κB and STING/IRF3 signalling, while TNF-α inhibition acted through the HMGB1/TLR4/MyD88/NF-κB axis 42480279Jul42219549May. Oxyphenbutazone targeted non-canonical inflammasome-mediated pyroptosis near caspase-11 and also inhibited canonical NLRP3 activation near caspase-1, largely independently of COX-1/2 42150290May. Tuolitounong Decoction reduced caspase-1, GSDMD, IL-1β, and IL-18 markers in granulomatous lobular mastitis models, although serotonin inhibition did not alter the model 42142128May. The work is therefore shifting toward upstream, disease-specific inflammasome intervention rather than glycemic, receptor-level, or broadly anti-inflammatory control alone.
Therapeutic Cell Death and Immunity: Anwulignan overcame proteasome inhibitor resistance in multiple myeloma by targeting NPM1 and activating the caspase-1-dependent GSDMD pyroptosis pathway 42704369Sep. GSDMD silencing weakened tumour suppression, while anwulignan increased T-cell proportions and promoted pyroptosis-driven immunogenic cell death in immunocompetent models 42704369Sep. A lung cancer review places pyroptosis alongside ferroptosis and necroptosis as immunogenic programmed cell death modalities that can convert immune-resistant tumours from “cold” to “hot” states 41998294Apr. This field is moving toward combining pyroptosis-inducing treatments with immunotherapy to overcome drug resistance and strengthen antitumour immunity.
Written from 11 PubMed abstracts, each one cited by PMID above. Published: 2026-08-28. Last written: 2026-09-09 by GPT. Drafted by language models from published abstracts; not medical advice.