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Ischemic stroke remains a leading cause of mortality and long-term disability worldwide. Although revascularization therapies have improved outcomes in certain patients, effective interventions for neurological deficits are still lacking. White matter injury plays a central role in driving persistent functional impairments. As the cellular foundation for myelin regeneration, oligodendrocyte precursor cells (OPCs) have emerged as a promising therapeutic target. This review systematically examines the pathophysiological alterations of OPCs following ischemic stroke, including their proliferation, migration, differentiation, and maturation into myelinating oligodendrocytes, and explores their dynamic interactions with the surrounding microenvironment, including microglia, astrocytes, neurons, and endothelial cells. Accumulating evidence indicates that OPCs not only facilitate myelin repair through differentiation into oligodendrocytes but also contribute to neuroprotection and vascular remodeling by secreting neurotrophic and pro-angiogenic factors. Therapeutic strategies aimed at preserving OPCs and enhancing their differentiation, including pharmacological therapy, cell transplantation, gene therapy, bioengineering and biomaterials technology, as well as rehabilitation and physical therapy, hold considerable promise for improving neurological recovery. By positioning OPC dysfunction as a driver of persistent disability, this review outlines a translational pathway toward therapies that restore white matter integrity and functional recovery after ischemic stroke.
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Wang et al. (2026) studied this question.
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