ArticleBlood2021
Gasdermin D inhibition prevents multiple organ dysfunction during sepsis by blocking NET formation.
Article in Blood, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers, 1 of them a synthesis that pooled it.
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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
173 citing papers in PubMed, 1 synthesis or guideline pooled it, 231 citations in OpenAlex.
- Review: the role of GSDMD in sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Pooled it
- METTL3 promotes neutrophil extracellular trap formation via SYK/ERK/MEK signaling during acute lung injury.Journal of advanced research · 2026Article
- The NLRP3 inflammasome in physiological and dysfunctional host response in human sepsis and critical illness: a narrative review.Critical care (London, England) · 2026Review
- Neutrophil extracellular traps in thrombosis of hematologic malignancies: Underlying mechanisms and therapeutic opportunities (Review).International journal of molecular medicine · 2026Review
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- EGFR orchestrates neutrophil activation and NETosis via CEBPβ-dependent PGLYRP1 induction.Cell death and differentiation · 2026Article
- Gasdermin D-Mediated Release of IL-33 Results in Fetal Brain Developmental Abnormalities During Maternal Colitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ERK/Smurf1 regulates non-canonical pyroptosis by prompting Caspase-11 ubiquitination.Cell death and differentiation · 2026Article
- Research progress on neutrophil extracellular traps in sepsis‑induced coagulopathy (Review).Molecular medicine reports · 2026Review
- NINJ1 plays a vital role in the release of neutrophil extracellular traps during acute lung injury.Cell death & disease · 2026Article
- A 'Tangled Web' in the CNS: unraveling neutrophil extracellular traps in neurological disorders.Molecular neurodegeneration · 2026Review
- Gasdermin D-dependent neutrophil pyroptosis exacerbates Coxsackievirus A6-induced neuroinflammation through NET formation.Journal of neuroinflammation · 2026Article
- New Insights Into the Role of Neutrophils in Lymphoma.Cancer medicine · 2026Review
- Biomimetic Targeted Drug Delivery for Liver Failure in Abdominal Sepsis: Focus on Autologous Erythrocyte Ghosts.International journal of molecular sciences · 2026Review
- Targeting pyroptosis in renal fibrosis: From molecular mechanisms to therapeutic horizons (Review).International journal of molecular medicine · 2026Review
- Neutrophil extracellular traps in the tumor microenvironment, metastasis, therapy, and beyond: advances, challenges, and perspectives.Journal of hematology & oncology · 2026Review
- Excessive pyroptosis mediates the exacerbation of pneumonia caused by low-lethality influenza virus and secondary MRSA co-infection.Cell death discovery · 2026Article
- Pharmacological Targeting of CXCR4 Attenuates Sepsis-Induced Intestinal Injury by Suppressing NLRP3/GSDMD-Mediated Pyroptosis.Inflammation · 2026Article
- Nanotherapeutic Macrophage-Neuro Reprogramming Through Immunometabolic Crosstalk Mitigates Sepsis-Induced Lung Injury and Neurologic Damage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- FDA-approved drug library screen identifies antidepressants, antimicrobials, anti-COPD, and anti-CVD agents as blockers of NLRP3 inflammasome and sepsis in a sex-dependent manner.bioRxiv : the preprint server for biology · 2026Article
113 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
27 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple organ dysfunction is the most severe outcome of sepsis progression and is highly correlated with a worse prognosis. Excessive neutrophil extracellular traps (NETs) are critical players in the development of organ failure during sepsis. Therefore, interventions targeting NET release would likely effectively prevent NET-based organ injury associated with this disease. Herein, we demonstrate that the pore-forming protein gasdermin D (GSDMD) is active in neutrophils from septic humans and mice and plays a crucial role in NET release. Inhibition of GSDMD with disulfiram or genic deletion abrogated NET formation, reducing multiple organ dysfunction and sepsis lethality. Mechanistically, we demonstrate that during sepsis, activation of the caspase-11/GSDMD pathway controls NET release by neutrophils during sepsis. In summary, our findings uncover a novel therapeutic use for disulfiram and suggest that GSDMD is a therapeutic target to improve sepsis treatment.
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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.