ReviewFrontiers in cell and developmental biology2026
Spatiotemporal and metabolic heterogeneity of tumor-associated macrophages in glioblastoma: from single-cell insights to therapeutic targeting.
Review in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- TREM2 in glioma: Reprogramming the immune microenvironment from mechanistic understanding to clinical translation (Review).Molecular medicine reports · 2026Review
- Polymeric Nano Drug Delivery Systems for Overcoming Tumor Microenvironment-Mediated Drug Resistance.Pharmaceutics · 2026Review
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Authors and funding
10 authors.
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Abstract
The immunosuppressive and therapy-resistant nature of glioblastoma (GBM) is fundamentally driven by the profound spatiotemporal and metabolic heterogeneity of tumor-associated macrophages (TAMs). This review proposes a spatiotemporal-metabolic axis as an integrative framework to decipher the functional plasticity of TAMs and its therapeutic implications. Drawing on the latest single-cell and spatial multi-omics data, we first delineate the lineage competition landscape of TAMs. Within this landscape, brain-resident microglia, border-associated macrophages (BAMs), and peripherally recruited bone marrow-derived macrophages (BMDMs) engage in dynamic interplay during tumor evolution, culminating in a shifted ecosystem dominated by BMDMs at recurrence. These subsets are not randomly distributed but are spatially organized through niche-instructive signals-such as hypoxia, perivascular cues, and tumor-derived metabolites-leading to context-dependent enrichment: immunosuppressive TAMs accumulate in the tumor core, BAMs localize to perivascular zones and express pro-angiogenic factors, while hypoxic necrotic regions are populated by metabolically reprogrammed HMOX1
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