ArticleRedox biology2025
Hydrogen sulfide inhibits recruitment of monocyte-derived tumor associated macrophages in glioblastoma by downregulating CXCL12.
Article in Redox biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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
3 citing papers in PubMed.
- Macrophage pyroptosis drives luminal senescence and club-cell reprogramming in 5α-reductase inhibitor-treated prostatic hyperplasia.Experimental & molecular medicine · 2026Article
- Research Progress on Novel Lead Compounds for Central Nervous System Diseases.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Heterogeneity, Measurement, and Clinical Implications of Oxygenation, Cell Signaling, and Redox Biology in Glioblastoma and Adult Diffuse Gliomas, with Context from Other Brain Tumors.Antioxidants (Basel, Switzerland) · 2026Review
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Tumor associated macrophages (TAMs) directly contribute to the dismal prognosis of glioblastoma by preventing anti-tumor immunity and promoting tumor invasion and angiogenesis. Inhibiting TAM infiltration is a potential therapeutic strategy in glioblastoma, with several chemokine antagonists in early clinical development. Hydrogen sulfide, a gasotransmitter that regulates microglial accumulation in a wide range of CNS diseases, may be a novel therapeutic target to prevent TAM recruitment in glioblastoma. In this study, hydrogen sulfide concentrations were directly measured from 14 isocitrate dehydrogenase (IDH)-wildtype glioblastoma surgical samples and compared against overall survival as well as expression of TAM markers and chemokines. Effects of hydrogen sulfide donor therapy on survival and TAM recruitment were also examined in a genetically engineered mouse model of glioblastoma. High hydrogen sulfide concentrations conferred a survival benefit in IDH-wildtype glioblastoma, in association with reduced monocyte-derived TAM density and downregulation of CXCL12. These findings were validated by administering hydrogen sulfide donor SG1002 to an immunocompetent mouse model of glioblastoma, which improved survival, inhibited monocyte infiltration, and downregulated CXCL12. Finally, hydrogen sulfide donor treatment directly reduced CXCL12 expression in glioblastoma cells, diminishing their ability to recruit monocytes in vitro. Taken together, these results demonstrate that hydrogen sulfide signaling prevents monocyte-derived TAM accumulation in glioblastoma by inhibiting chemotaxis.
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Registered trials
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