ArticleNature communications2021
Inflammasome-mediated GSDMD activation facilitates escape of Candida albicans from macrophages.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 2 of them syntheses that pooled it.
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.
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
69 citing papers in PubMed, 2 syntheses or guidelines pooled it, 96 citations in OpenAlex.
- Mitochondria: a breakthrough in combating rheumatoid arthritis.Frontiers in medicine · 2024Pooled it
- Review: the role of GSDMD in sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Pooled it
- The ubiquitin-editing enzyme A20 (TNFAIP3): mechanisms of activation, biological function, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- ROS-Dependent GSDMD Activation Drives Intestinal Pyroptosis in Neonatal Necrotizing Enterocolitis (NEC).Cell biology international · 2026Article
- The transcription factor Ahr1 governs the recruitment of neutrophils to the brain and clearance ofmBio · 2026Article
- Transdifferentiated BLaER1 cells as a genetically tractable model to study the interaction of pathogenic fungi with macrophages.Disease models & mechanisms · 2026Article
- Dangerous liaisons: Candidalysin and myeloid cells in candidiasis.PLoS pathogens · 2026Article
- The challenge of cell death switching in inflammasome-targeted therapies for bacterial and viral infections.Communications biology · 2026Review
- Infection-induced glucose starvation triggers NINJ1-dependent macrophage lysis and Candida escape.Nature communications · 2026Article
- Diabetes and Immunosuppression Drive Distinct Patterns ofbioRxiv : the preprint server for biology · 2026Article
- Multidimensional assessment of in-host fitness costs of echinocandin resistance in the opportunistic fungal pathogenAntimicrobial agents and chemotherapy · 2026Article
- Delayed disulfiram targeting GSDMD-NETs axis rescues sepsis by limiting bacterial spread and lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Synthetic Lethal Therapy Based on Dimorphism for Systemic Infection of Drug-Resistant Candida albicans.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Tubule-Derived IFN-α Promotes GSDMD-Mediated Macrophage Pyroptosis to Drive Renal Inflammation and Fibrosis Through JAK2/STAT2 Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Inflammasomes meet organoids and artificial intelligence: unraveling the complexity of gynecological inflammation.Frontiers in immunology · 2026Review
- Candidalysin at the epithelial-systemic interface: mechanistic evidence, critical-care relevance, and translational opportunities in invasive candidiasis.Frontiers in cellular and infection microbiology · 2026Review
- Comparative progress on the mechanisms of airway mucosal injury induced by different pathogens: SARS-CoV-2, influenza A virus, and Mycoplasma pneumoniae.Frontiers in cellular and infection microbiology · 2026Review
- GSDMD deficiency attenuates BPD by suppressing macrophage pyroptosis and promoting M2 polarization.Cell death discovery · 2025Article
- Cytosolic receptors and signaling in antifungal immunity.The EMBO journal · 2025Review
- Human non-canonical inflammasomes activate CASP3 to limit intracellularbioRxiv : the preprint server for biology · 2025Article
9 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
19 authors at 3 institutions in 2 countries.
Funding
Abstract
Candida albicans is the most common cause of fungal sepsis. Inhibition of inflammasome activity confers resistance to polymicrobial and LPS-induced sepsis; however, inflammasome signaling appears to protect against C. albicans infection, so inflammasome inhibitors are not clinically useful for candidiasis. Here we show disruption of GSDMD, a known inflammasome target and key pyroptotic cell death mediator, paradoxically alleviates candidiasis, improving outcomes and survival of Candida-infected mice. Mechanistically, C. albicans hijacked the canonical inflammasome-GSDMD axis-mediated pyroptosis to promote their escape from macrophages, deploying hyphae and candidalysin, a pore-forming toxin expressed by hyphae. GSDMD inhibition alleviated candidiasis by preventing C. albicans escape from macrophages while maintaining inflammasome-dependent but GSDMD-independent IL-1β production for anti-fungal host defenses. This study demonstrates key functions for GSDMD in Candida's escape from host immunity in vitro and in vivo and suggests that GSDMD may be a potential therapeutic target in C. albicans-induced sepsis.
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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.