ArticleCell death & disease2023
Gasdermin D-mediated pyroptosis is regulated by AMPK-mediated phosphorylation in tumor cells.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 27 citations in OpenAlex.
- The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 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
- Kinetic control of macrophage death by PTM-turnover crosstalk in infection and inflammation.Cell chemical biology · 2026Review
- Pyroptosis: Turning Up the Heat on Cancer.Annual review of immunology · 2026Review
- A novel Chinese medicine formula against hyperuricemia-induced kidney inflammation involving pyroptosis inhibition via modulating AMPK-TLR4-NLRP3 pathway.Chinese medicine · 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
- Triptolide in Combination with the Gli1 Inhibitor GANT61 Eradicates Anaplastic Thyroid Cancer by Suppressing Cancer Stem Cell Self-Renewal and Enhancing Apoptosis and Pyroptosis.International journal of biological sciences · 2026Article
- p53 Orchestrates the Immunogenic-Tolerogenic Pyroptosis Switch in Non-Small Cell Lung Cancer: A Systems Biology Approach.Computational and structural biotechnology journal · 2026Article
- Disulfiram Attenuates Bleomycin-Induced Lung Inflammation and Fibrosis with Reduced Endothelial Pyroptosis and Neutrophil Adhesion.Journal of inflammation research · 2026Article
- Pyroptosis in premature ovarian insufficiency: pathogenic mechanisms, pathway crosstalk, and therapeutic strategies.Frontiers in medicine · 2026Review
- AMPK-PP1/PP2 axis regulates GSDMD-mediated pyroptosis via phosphorylation.Frontiers in oncology · 2026Article
- To Die or Not to Die: How Sublethal Damage Rewires Cell Fate and Implications for Sepsis.Journal of inflammation research · 2026Review
- Gasdermins in neurodegeneration: emerging mechanisms and therapeutic targets.Cell death & disease · 2025Review
- Exploring cell death pathways in oral cancer: mechanisms, therapeutic strategies, and future perspectives.Discover oncology · 2025Review
- GSDMD-mediated mitochondrial dysfunction in marginal cells: A potential driver of inflammation and stria vascularis damage in CIHL.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Ubiquitination of gasdermin D N-terminal domain directs its membrane translocation and pore formation during pyroptosis.Cell death & disease · 2025Article
- Exploiting gasdermin-mediated pyroptosis for enhanced antimicrobial activity of phage endolysin againstmSystems · 2025Article
- The conflicting role highlights the complexity of GSDMs in cancer.Frontiers in immunology · 2025Review
- Investigation of Active Components ofInternational journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Gasdermin D (GSDMD) is a critical mediator of pyroptosis, which consists of a N-terminal pore-forming domain and a C-terminal autoinhibitory domain. Its cytolytic activity is sequestered by the intramolecular autoinhibitory mechanism. Upon caspase-1/11 mediated cleavage of GSDMD, the N-terminal pore-forming domain (GD-NT) is released to mediate pyroptosis. However, it remains unclear how GD-NT is regulated once it is generated. In the current study, we developed a TetOn system in which GD-NT was selectively induced in tumor cells to explore how the cytolytic activity of GD-NT is regulated. We found that the cytolytic activity of GD-NT was negatively regulated by the AMP-activated protein kinase (AMPK) and AMPK activation rendered tumor cells resistant to GD-NT-mediated pyroptosis. Mechanistically, AMPK phosphorylated GD-NT at the serine 46 (pS46-GD), which altered GD-NT oligomerization and subsequently eliminated its pore-forming ability. In our in vivo tumor model, AMPK-mediated phosphorylation abolished GD-NT-induced anti-tumor activity and resulted in an aggressive tumor growth. Thus, our data demonstrate the critical role of AMPK in negatively regulating the cytolytic activity of GD-NT. Our data also highlight an unexpected link between GSDMD-mediated pyroptosis and the AMPK signaling pathway in certain tumor cells.
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