ArticleNeural regeneration research2026
Physical exercise promotes white matter repair after ischemic stroke.
Article in Neural regeneration research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Microglia and neuroinflammation: function, heterogeneity, and crosstalk.Cellular & molecular immunology · 2026Review
- The neuro-immuno-metabolic axis of exercise: a unified mechanistic framework for exercise-induced cognitive enhancement and psychological resilience.Frontiers in psychology · 2026Review
- Regulatory T cells in bullous pemphigoid: biological characteristics, dysfunction, and pathogenic roles.Frontiers in immunology · 2026Review
- Regulatory T cells promote microglia-mediated synapse engulfment and functional recovery via the OPN-CD74 axis after spinal cord injury in mice.Journal of neuroinflammation · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
JOURNAL/nrgr/04.03/01300535-202606000-00053/figure1/v/2026-02-11T151048Z/r/image-tiff White matter injury is a key factor impacting stroke recovery. Physical exercise can promote white matter repair. Immune cells, especially regulatory T (Treg) cells, contribute to strengthening white matter integrity, yet little is known about the underlying mechanism. To examine this, we established a transient middle cerebral artery occlusion male mouse model. We found that physical exercise elevated brain Treg cells, thereby enhancing neurological recovery, reducing neuroinflammation, promoting myelin debris clearance, and accelerating white matter repair. Depletion of Treg cells caused a decrease in these positive effects of physical exercise. Mechanistically, the rise in osteopontin triggered by physical exercise is dampened when Treg cells are depleted. In addition, Treg-conditioned medium reduced oxygen-glucose deprivation/re-oxygenation-induced microglial inflammation and enhanced phagocytosis, which could be blocked by osteopontin antibodies. Importantly, although Treg infusion could mimic the protective effects of physical exercise, osteopontin blockade partially countered the effects of physical exercise and Treg cells. Finally, our sequencing data revealed a marked upregulation of C-X-C motif chemokine ligand 12 (CXCL12) mRNA expression subsequent to physical exercise, which was confirmed at the protein level. Stimulation of Treg cells with stroke brain lysates increased C-X-C motif chemokine receptor 4 (CXCR4) expression, indicating a potential role for the CXCL12-CXCR4 axis in recruiting Treg cells. These findings suggest that physical exercise promotes white matter repair after ischemic stroke by Treg cells.
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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 OpenQuestion graph.