ArticleJournal of inflammation research2026
Astrocytes and Microglia Regulate Opioid Receptor-Driven Cancer Brain Metastasis and Neural Injury: Remodeling the Brain Microenvironment.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Spatial omics of neuroinflammation: insights across brain diseases.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain metastasis is a common complication in the progression of multiple solid tumors and is associated with poor prognosis. Its occurrence is not determined solely by the intrinsic invasiveness of tumor cells. After tumor cells enter the central nervous system (CNS), their survival and expansion largely depend on the brain microenvironment. Circulating tumor cells (CTCs) must first cross the blood-brain barrier (BBB). They then encounter a defensive microenvironment centered on reactive astrocytes and disease-associated microglia. This "colonization bottleneck" prevents most disseminated cells from surviving. Under tumor-derived stimulation, neuroglial cells undergo functional reprogramming. They shift from a predominantly restrictive state to a tumor-supportive adaptive state. This shift involves amplified inflammation, enhanced immunosuppression, and altered metabolic coupling, which together reshape the metastatic niche in the brain. At the same time, disruption of microenvironmental homeostasis affects neuronal survival. This links brain metastasis with neuronal injury. Opioid receptors (ORs) are functionally expressed in astrocytes and microglia. Their activation regulates inflammatory responses, metabolic states, and immune signaling networks. They may serve as key signaling nodes that control functional shifts in neuroglial cells. Opioid receptor signaling does not directly drive tumorigenesis. Instead, it likely resets how neuroglial cells respond to external perturbations. This process amplifies brain microenvironmental dysregulation. As a result, it indirectly promotes brain metastatic colonization and aggravates neuronal injury. In summary, brain metastasis results from long-term interactions between tumor cells and the brain microenvironment. Elucidating glia-mediated selection mechanisms and their regulatory nodes will deepen the understanding of the biological nature of brain metastasis.
Indexed as
Identifiers
What OpenQuestion holds
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.