ArticleNature communications2026
Infection-induced glucose starvation triggers NINJ1-dependent macrophage lysis and Candida escape.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed.
- NINJ1: implications for plasma membrane rupture and disease.Biochemical Society transactions · 2026Review
- Transdifferentiated BLaER1 cells as a genetically tractable model to study the interaction of pathogenic fungi with macrophages.Disease models & mechanisms · 2026Article
- Candidalysin at the epithelial-systemic interface: mechanistic evidence, critical-care relevance, and translational opportunities in invasive candidiasis.Frontiers in cellular and infection microbiology · 2026Review
- Fungal determinants contributing to translocation ofmicroLife · 2025Article
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Authors and funding
24 authors.
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Abstract
Pathogens compete for glucose with macrophages, which disrupts host glycolysis, modulates antimicrobial responses and causes macrophage death. We show that glucose starvation induced by major fungal pathogens Candida albicans and Candida auris causes macrophage lysis by activating NINJ1, the executioner of membrane rupture during cell death. In glucose-starved macrophages, NINJ1 ruptures membranes independently of known cell death programs. Consistently, NINJ1 is the dominant effector of fungal-induced macrophage damage amongst host cell death factors. Supplementation of the amino acid alanine rescues glucose-starved macrophages better than glucose, and it does so by inhibiting NINJ1 oligomerization. Moreover, C. albicans infection disrupts amino acid metabolism in mice and reduces serum alanine. Finally, NINJ1-mediated membrane rupture enables C. albicans egress from macrophages together with the toxin candidalysin. We establish the mechanism of glucose starvation-induced macrophage damage by NINJ1, and demonstrate the roles of NINJ1 and alanine in immune responses to Candida and fungal escape.
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