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Immature brain-supporting cells switch fate to restore blood flow after stroke

10.30.25 | International Society for Stem Cell Research

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Stroke is a leading cause of death and disability, affecting 1 in 4 people during their lifetime. Stroke happens when blood vessels in the brain get clogged or damaged, impairing blood flow and oxygen supply to the brain, which leads to death of neurons and other brain cells. Although brain damage can be limited by interventions to restore blood flow, most stroke survivors experience some lifelong impairments of e.g. speech, movement, or cognitive function.

Despite the existence of immature stem cells in the brain, their role in repair is uncertain and the brain’s ability to recover from stroke remains limited. Takakuni Maki, Ken Yasuda, Kazuto Tsukita, and colleagues from Kyoto University , Japan, have now demonstrated that oligodendrocyte progenitor cells (OPCs)—a well-known immature glial cell type in the brain—can promote new blood vessel formation after stroke under hypoxic conditions. The research was published today in Stem Cell Reports .

The researchers found that OPCs, whose normal task is to differentiate into oligodendrocytes that form an insulating layer around axons to support neuronal function, among other roles, can change their behavior under conditions of extremely low oxygen, such as in stroke areas in the brain, and start to interact with blood vessels to stimulate their growth. The researchers were able to demonstrate this connection when they exposed mouse OPCs in the lab to very low oxygen levels simulating stroke. When injected into the blood circulation of mice with stroke, the OPCs migrated to the stroke region and survived there for several weeks. Critically, the low oxygen-conditioned OPCs more effectively helped to limit the damage to brain tissue and partially restored movement and behavior compared with unconditioned OPCs. This was likely due to the extensive formation of new blood vessels, which is critical for restoring oxygen and nutrient supply to brain cells, found in stroke brains treated with low oxygen-conditioned OPCs.

More research will be required to confirm these results and test if low oxygen-conditioned OPCs are safe and effective to be used in patients, potentially in combination with standard interventions to promote blood flow and re-oxygenation.

About Stem Cell Reports
Stem Cell Reports is the open access, peer-reviewed journal of the International Society for Stem Cell Research (ISSCR) for communicating basic discoveries in stem cell research, in addition to translational and clinical studies. Stem Cell Reports focuses on original research with conceptual or practical advances that are of broad interest to stem cell biologists and clinicians. Stem Cell Reports is a Cell Press partner journal. Find the journal on X: @StemCellReports .

About ISSCR
With nearly 5,000 members from more than 80 countries, the International Society for Stem Cell Research ( @ISSCR ) is the preeminent global, cross-disciplinary, science-based organization dedicated to stem cell research and its translation to the clinic. The ISSCR mission is to promote excellence in stem cell science and applications to human health.

Stem Cell Reports

10.1016/j.stemcr.2025.102687

Characterizing hypoxia-orchestrated post-stroke changes in oligodendrocyte precursor cells for optimized cell therapy

30-Oct-2025

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Article Information

Contact Information

Kym Kilbourne
International Society for Stem Cell Research
kkilbourne@isscr.org

How to Cite This Article

APA:
International Society for Stem Cell Research. (2025, October 30). Immature brain-supporting cells switch fate to restore blood flow after stroke. Brightsurf News. https://www.brightsurf.com/news/1ZZ0MWR1/immature-brain-supporting-cells-switch-fate-to-restore-blood-flow-after-stroke.html
MLA:
"Immature brain-supporting cells switch fate to restore blood flow after stroke." Brightsurf News, Oct. 30 2025, https://www.brightsurf.com/news/1ZZ0MWR1/immature-brain-supporting-cells-switch-fate-to-restore-blood-flow-after-stroke.html.