ArticleCell reports2023
Gasdermin D pore-forming activity is redox-sensitive.
Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 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.
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Who cites it
89 citing papers in PubMed, 120 citations in OpenAlex.
- The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Igniting antitumour immunity with cancer cell pyroptosis.Nature reviews. Cancer · 2026Review
- Article
- Structural basis of GSDME pore formation and its regulation by S-palmitoylation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Targeting Gasdermins for Therapeutic Interventions in Central Nervous System Injury.Neurotoxicity research · 2026Review
- Osteocyte-specific gasdermin D deletion accelerates osteoarthritis via promoting subchondral inflammation and remodeling.Bone research · 2026Article
- Gasdermin D in Neurodegenerative Diseases: Pathogenic Roles and Therapeutic Perspectives.Molecular neurobiology · 2026Review
- β-catenin-driven innate and metabolic reprograming in macrophages fuel T-cell-dependent inflammation in Toxoplasma gondii infection: implications for therapeutic intervention.Cell death & disease · 2026Article
- Development of a novel GAK solution for efficient hypothermic preservation of NK cell viability and anti-tumor function.Stem cell research & therapy · 2026Article
- Tailored Porous Bimetallic Nanozyme Platform for Full-Cycle Therapeutics of Intestinal Ischemia/Reperfusion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- d-amino acids restrain macrophage IL-1β release through gasdermin D acetylation.Science advances · 2026Article
- Long-Term Static Cultivation Alters Lipid Metabolism and Bioenergetic Capacity in A549 Cells.International journal of molecular sciences · 2026Article
- Redox Regulation of the NLRP3 Inflammasome and its Implications for Immunization-related Neuroinflammation.Molecular neurobiology · 2026Review
- Palmitoylation-dependent regulation of innate and adaptive immunity: molecular insights and translational opportunities.Cellular & molecular biology letters · 2026Review
- Reactive oxygen species (ROS) in cancer: from mechanism to therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Environmental Amino Acid Sensing Regulates the Rate of ASC Translation and NLRP3 Inflammasome Assembly.bioRxiv : the preprint server for biology · 2026Article
- Gasdermin D Cleavage and Cytokine Release, Indicative of Pyroptotic Cell Death, Induced by Ophiobolin A in Breast Cancer Cell Lines.International journal of molecular sciences · 2026Article
- Disulfiram Attenuates Bleomycin-Induced Lung Inflammation and Fibrosis with Reduced Endothelial Pyroptosis and Neutrophil Adhesion.Journal of inflammation research · 2026Article
- Delving into pyroptosis in atherosclerosis: role, mechanisms and therapeutic opportunities.Frontiers in immunology · 2026Review
- To Die or Not to Die: How Sublethal Damage Rewires Cell Fate and Implications for Sepsis.Journal of inflammation research · 2026Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Reactive oxygen species (ROS) regulate the activities of inflammasomes, which are innate immune signaling organelles that induce pyroptosis. The mechanisms by which ROS control inflammasome activities are unclear and may be multifaceted. Herein, we report that the protein gasdermin D (GSDMD), which forms membrane pores upon cleavage by inflammasome-associated caspases, is a direct target of ROS. Exogenous and endogenous sources of ROS, and ROS-inducing stimuli that prime cells for pyroptosis induction, promote oligomerization of cleaved GSDMD, leading to membrane rupture and cell death. We find that ROS enhance GSDMD activities through oxidative modification of cysteine 192 (C192). Within macrophages, GSDMD mutants lacking C192 show impaired ability to form membrane pores and induce pyroptosis. Reciprocal mutagenesis studies reveal that C192 is the only cysteine within GSDMD that mediates ROS responsiveness. Cellular redox state is therefore a key determinant of GSDMD activities.
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What OpenQuestion holds
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.