ArticleCell reports2025
Neuropeptide adrenomedullin remodels stemness and macrophage dynamics in glioblastoma.
Article in Cell reports, 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.
- Galanin impairs tumor immunity in glioblastoma by promoting infiltration and ferroptosis resistance of myeloid-derived suppressor cells.Nature cancer · 2026Article
- Macrophage-Fibroblast Crosstalk Shapes Wound Repair Signaling In Vitro.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Symbiotic exclusivity between CLOCK and TFPI2 drives stemness and immunosuppression in glioblastoma models.The Journal of clinical investigation · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
The presence of self-renewing glioblastoma (GBM) stem cells (GSCs) and infiltrating pro-tumor macrophages constitutes two key hallmarks of GBM. Here, we identified the neuropeptide adrenomedullin (ADM) as a key factor regulating GSC-macrophage symbiosis. Epidermal growth factor receptor (EGFR) overexpression upregulates ADM in GSCs to enhance their self-renewal, glycolysis, and tumor growth by activating the signal transducer and activator of transcription 3 (STAT3) pathway. GSC-secreted ADM promotes macrophage infiltration and pro-tumor reprogramming through activation of ADM receptor (ADMR), thereby engaging both STAT3 and STAT6 pathways. In GBM mouse and patient-derived xenograft (PDX) models, inhibition of the ADM-ADMR axis, STAT3, or STAT6 suppresses tumor progression, GSC self-renewal, and pro-tumor macrophage abundance, with dual inhibition of STAT3 and STAT6 leading to durable complete tumor regression in a subset of tumor-bearing mice. In human GBM tumors and plasmas, ADM correlates positively with GSC stemness, pro-tumor macrophage abundance, and poor prognosis. These findings highlight ADM-triggered GSC-macrophage symbiosis as a promising therapeutic target for GBM.
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Registered trials
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