ArticleNature immunology2021
Intracellular immune sensing promotes inflammation via gasdermin D-driven release of a lectin alarmin.
Article in Nature immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 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
86 citing papers in PubMed, 124 citations in OpenAlex.
- The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 2026Review
- The NLRP3 inflammasome in physiological and dysfunctional host response in human sepsis and critical illness: a narrative review.Critical care (London, England) · 2026Review
- Unanchored ubiquitin chains promote the non-canonical inflammasome via UBXN1.Research square · 2026Article
- Glycoprotein-induced phase separation drives unconventional secretion of galectin-3.Nature communications · 2026Article
- Multifactorial effects of LGALS1 blockade sensitize tumors to immune checkpoint inhibitor.Experimental hematology & oncology · 2026Article
- Mesenchymal stem cell-derived small extracellular vesicles suppress pyroptosis by delivering miR-125a-5p to improve acute kidney injury in sepsis.Cell death discovery · 2026Article
- Redefining Shiga toxin-induced human cell death as NLRP1- and gasdermin E-mediated pyroptosis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- LPS-induced structural reorganization and polymerization drive noncanonical inflammasome activation.Science advances · 2026Article
- S100A12 drives inflammatory and metabolic reprogramming in sepsis-associated acute kidney injury.Frontiers in molecular biosciences · 2026Review
- Gasdermin D-driven pyroptosis in sepsis: mechanisms, therapeutic strategies, and clinical translation.Frontiers in immunology · 2026Review
- The gene regulatory networks shaping macrophage plasticity and altered function in fibrosis.Frontiers in immunology · 2026Review
- The TP53-LGALS4 axis modulates the tumor immune microenvironment and synergizes with anti PD-L1 therapy in colorectal cancer.Journal of translational medicine · 2025Article
- Organelles and cancer cell pyroptosis: overview and perspectives.Cell death & disease · 2025Review
- Qing-Re-Xiao-Zheng-yi-qi formula protects renal function by stabilizing lysosomal membranes and inhibiting NLRP3-inflammasome-mediated pyroptosis in diabetic kidney disease.Annals of medicine · 2025Article
- Gasdermins: multifunctional effectors of membrane permeabilization across cellular compartments.The FEBS journal · 2025Review
- Time-resolved monitoring of yeast responses to lipopolysaccharide exposure by cell-released volatile organic compounds.Applied and environmental microbiology · 2025Article
- Endolysosomal damage surveillance enables rapid inflammasome sensing of pathogens.Cell reports · 2025Article
- Cell death signaling and immune regulation: new perspectives on targeted therapy for sepsis.Cellular & molecular biology letters · 2025Review
- Tumor glyco-immunology, glyco-immune checkpoints and immunotherapy.Journal for immunotherapy of cancer · 2025Review
- Functional Materials Targeted Regulation of Gasdermins: From Fundamentals to Functionalities and Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 5 institutions in 3 countries.
Funding
Abstract
Inflammatory caspase sensing of cytosolic lipopolysaccharide (LPS) triggers pyroptosis and the concurrent release of damage-associated molecular patterns (DAMPs). Collectively, DAMPs are key determinants that shape the aftermath of inflammatory cell death. However, the identity and function of the individual DAMPs released are poorly defined. Our proteomics study revealed that cytosolic LPS sensing triggered the release of galectin-1, a β-galactoside-binding lectin. Galectin-1 release is a common feature of inflammatory cell death, including necroptosis. In vivo studies using galectin-1-deficient mice, recombinant galectin-1 and galectin-1-neutralizing antibody showed that galectin-1 promotes inflammation and plays a detrimental role in LPS-induced lethality. Mechanistically, galectin-1 inhibition of CD45 (Ptprc) underlies its unfavorable role in endotoxin shock. Finally, we found increased galectin-1 in sera from human patients with sepsis. Overall, we uncovered galectin-1 as a bona fide DAMP released as a consequence of cytosolic LPS sensing, identifying a new outcome of inflammatory cell death.
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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.