ReviewJournal of neuroinflammation2026
The immunoproteasome as a neuroimmune hub in the central nervous system: from proteostasis stress to inflammatory pathology.
Review in Journal of neuroinflammation, 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.
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
Abstract
The immunoproteasome (IP) is a stress-inducible specialization of the ubiquitin-proteasome system that integrates immune activation with cellular homeostasis in the central nervous system (CNS). Incorporation of the inducible β1i, β2i, and β5i subunits enhances proteolytic capacity under inflammatory, oxidative, and metabolic stress, thereby supporting redox balance, mitochondrial integrity, and proteostasis. IP expression is highly dynamic and cell type-specific, varying across astrocytes, microglia, endothelial cells, and neurons in response to local microenvironmental cues. Functionally, IP activation exhibits a dual nature: transient induction facilitates the clearance of damaged proteins and fine-tunes inflammatory signaling, whereas sustained or dysregulated activation reinforces NF-κB- and STAT-dependent inflammatory programs, disrupts proteostatic equilibrium, and increases neuronal and vascular vulnerability. Across neurological disorders, the IP acts as a context-dependent regulator, shaping post-ischemic inflammation and blood-brain barrier (BBB) integrity, contributing to maladaptive responses in Alzheimer’s and Parkinson’s disease, and amplifying immune-mediated injury in multiple sclerosis, neuromyelitis optica spectrum disorder, epilepsy, and infectious encephalitis. Elucidating the spatiotemporal regulation of the IP and its therapeutic selectivity may enable precision immunomodulatory strategies for CNS diseases.
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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 Socratic graph.